Welcome, everyone, to the 44th Annual JP Morgan Healthcare Conference. My name is Anupam Rama. I'm one of the senior biotech analysts here at JP Morgan. I'm joined by my squad, Joyce Zhou, Priyanka Grover, and Rathi Pinhey. Our next presenting company is Maze Therapeutics, and presenting on behalf of the company, we have CEO Jason Coloma. Jason?
Good morning, everyone. I'm Jason Coloma. I'm the CEO of Maze Therapeutics, and first of all, I'd like to thank JP Morgan for having us at this year's conference. I'd also like to thank everyone that's in attendance today in the room, as well as those listening to the webcast. As Maze approaches its one-year anniversary as a publicly traded company, we are poised for a strong 2026, and I'd also like to thank Anupam and the team for being supportive in our transition to being a public company, as we've been benefiting, of course, from the recent progress that we've been having in terms of our pipeline. I'd also like to acknowledge our forward-looking statements. At Maze Therapeutics, our mission is simple yet ambitious: to harness the power of human genetics to transform the lives of patients. Kidney disease is a silent killer. It's a growing global epidemic issue.
37 million people in the U.S. alone suffer from kidney disease. It's the ninth leading cause of death globally now. In some countries, there's at least a four-year waiting list for a kidney transplant. There are no precision medicines approaches. There have been very little innovation, and that's where we fit in. At Maze Therapeutics, we are using our cutting-edge genetics approaches, developing novel small-molecule precision medicines for kidney disease, and thus far, we've been making some great progress. I'm extremely proud of the slide that you see here, as it represents all of the hard work that our scientists have been able to accomplish over the years. We are a clinical stage company with multiple programs, with key catalysts in the short term, as well as anticipated milestones coming this year, starting with MZE829 for APOL1 kidney disease that I'll discuss in more detail.
What's important to reiterate here is that we are reiterating our guidance, and we are on track, status quo, to be able to deliver our top-line proof-of-concept data by the end of this quarter. Now, what is new is that we are providing more specific guidance on the cadence of our study on MZE782. Now, last fall, we reported some very strong data, both that reinforced the concept in PKU as well as in kidney disease. So, based off of that, and I would say just the tremendous enthusiasm that we have from the overall community, we are starting our PKU study by the middle of this year. That's new news, and we are starting our kidney disease program and that study by the end of 2026.
Now, we are in a strong capital position based off of the partnerships that we've been able to strike, as well as the financings over the years. We have operating capital into 2028, and based on that current business plan, we'll be able to support everything in terms of our near-term milestones, as well as the near-term catalysts. Now, let's start with MZE829, APOL1 kidney disease. Now, the genetics of APOL1 kidney disease were known for a very long time, but no one really understood the function by which APOL1 was causing disease. Now, it's a horrible disease that I'll talk about in just a second, but MZE829 represents what could be a tremendous breakthrough, as there are no approved therapies for APOL1 kidney disease, and we're on track to deliver that proof-of-concept data by the end of Q1 2026.
These are the key takeaways that I want you to have from MZE829. Now, this is being developed as a once-a-day therapy, and at least 250,000 individuals in the U.S. alone can benefit from that type of approach. We have data to support that MZE829 has a differentiated, if you will, best-in-class mechanism that allows it to be able to potentially work on a broad set of patients with APOL1-mediated kidney disease. We had strong phase I data that supported not only the ability to advance the program, having a good understanding of the dose that we've selected to really give us the opportunity and the chance to see an effect in broad AMKD, both with or without diabetes.
And if we see the data that we hope to see by the end of the quarter, we will be starting and initiating our planning for a phase IIB/III study that allows for multiple registration strategies as we think about the potential for eventual approval. Now, in terms of the APOL1-mediated kidney disease patient, who are they? Disproportionately affects the Black community. Now, when people think about kidney disease, they usually think about an elderly population. APOL1 kidney disease usually clinically presents before the age of 50, so they're younger. They have accelerated progression, so what that means is that they can transition to end-stage renal disease or even into dialysis up to 10 years even earlier than a person that doesn't have APOL1 kidney disease. And they're not, if you will, benefiting from the current standard of care.
The medicines that are available to date, there are no approved therapies specifically for this indication. What we hear from the community at large, including the kidney physicians, is that some of the patients, unfortunately, go into what you call crashing into dialysis. What that means is that a person could feel relatively healthy, and what they end up doing is, over some time, they end up going straight into dialysis. Unfortunately, I think many people in here in this room can kind of appreciate this or know someone who has gone into dialysis. It dramatically changes their lives. More importantly, we know that the outcomes of those individuals that go into dialysis are horrible in the sense that if I showed you a survival curve of someone that was in dialysis after 10 years, it'll look very similar to those that have metastatic breast cancer.
That's what it means to be a real silent killer in the sense of what we might be able to address. Now, with MZE829, our goal is to try to treat and address the underlying condition itself and being able to develop a therapy that goes after APOL1 itself. Now, there are at least 250,000 individuals who can benefit from such an approach. To think about this particular pie chart you see here, about 60% of them don't have diabetes. 40% have diabetes. That's important because that is the data that we will be trying to support at the end of this quarter. Our goal is to show an effect in particular in broad AMKD with or without diabetes. There are no approved therapies to date, and that is ultimately what we intend to do.
Now, to contextualize that particular number is to really think about other therapies. The therapy and an indication that you're probably more familiar with, ATTR-CM, is probably about half the number of patients that are available for this type of therapy. So it represents a significant need of APOL1 kidney disease patients, but again, there are no approved therapies, and our goal, of course, is to try to change that. Now, let's dive into the mechanism. So if you remember what a kidney actually does, it's all about filtering out the waste and the toxins that accumulate in your body. And so what ends up happening is that with APOL1 kidney disease is what you can see here on the left.
So it's caused by a particular genetic variant, and when it's overexpressed, these particular APOL1 pores that form that you can see here on the left, you can see these two vertical lines that embed themselves into the cell. Those basically are punching a hole into the cell, causing some damage. But not only are they punching a hole into the cell, they're also, if you will, allowing particular things, some bad actors, which are represented in the blue dots that you see here, that go into the cell and ultimately cause cellular damage and ultimately cellular death. So what you want to be able to do is what you see here on the left, which is basically this idea with the dual mechanism, what MZE829 is able to do. And I'm sorry, it's on the right.
What you want to be able to do is minimally be able to block the pore, so you're not allowing those blue dots or those bad actors to enter into the cell. But also, you want to be able to work upstream from that to stop the pores, if you will, from forming to begin with, ultimately reducing the number of things that are punching holes into those kidney cells and ultimately resulting in being able to, if you will, help the patients and no longer have disease. Now, we reported our phase I data in the 2024 seminal k idney conference ASN. We had solid data that supported our advancement into phase II. The first two panels are our SAD and MAD data, which really represent the fact that we know that we can treat this as a once-a-day therapy.
What you see here on the graph on the right is how we selected our dose for the phase II, being able to, if you will, be able to maximally inhibit the target that allows us to have the best chance to show an effect in broad AMKD. We had a favorable safety profile, and all of this data means at the end of the day that it really supported the advancement of the phase II into what we call our phase II study HORIZON. Now, HORIZON is our global phase II study that is ongoing and enrolling and is on track to deliver top-line proof-of-concept data by the end of this quarter. Now, a couple of things to highlight here on the left. What we're trying to do is enroll patients that start with the ability to genotype them, so they have two copies of this particular variant.
They have two copies of the variant. We treat them for three months, and then we follow them for a month. And in addition to looking at particular data, the key efficacy biomarker that we're looking at is called UACR, which is basically a measurement of how much protein is in your urine. It's a way, if you take lab tests, you're visiting your primary care physician, that they look and try to detect damage of your kidney. And so you want to be able to lower that number. Essentially, the lower, the better. And so if you look on the right, our initial cutoff in terms of that UACR level is at 300 mg/g . To put that into context, a healthy individual that has healthy kidneys, that's going to be below 30, so you want to be able to reduce that.
It's also important to note that at that 300 number, that gives us the best shot to have at least a quarter of a million individuals who can benefit from that particular therapy. Now, one of the goals of being able to try to run this study in our HORIZON study is to show at least a 30% reduction in UACR relative to baseline. That would be clinically meaningful. That threshold has been set not only in discussion with key opinion leaders in the kidney community, but as well as looking at talking to folks in academia. There's a group called PARASOL that has really informed us how to think about success here.
The idea and the key takeaways for everyone in terms of MZE829, number one, we hope to be the first company to describe clinical proof-of-concept in what's called broad AMKD with or without diabetes that could be at least 250,000 individuals in the U.S. We've defined success at least a 30% reduction of proteinuria relative to baseline. The third thing which is important is if we see that data that we hope to see by the end of the quarter, we would initiate our planning for a phase IIB/III study that really allows us to think about the registrational path as well as think about an eventual approval. Now, let's shift gears to MZE782, which is for a rare disease, a rare metabolic disease called PKU. Now, left untreated, it really does cause a lot of issues in the brain, including severe seizures.
There are therapies available for the patients, but unfortunately, not everyone is able to really reap a lot of benefit from those therapies. MZE782, as I walk you through it, provides an opportunity to work for almost all of the particular patients that have the disease and, more importantly, could really fundamentally change the way that they live their lives. Now, a healthy individual that's on a standard Western diet usually has about 100 g. That's usually what people have if you're living what would be more of a standard Western diet. A PKU patient, on the other hand, can only have up to 10 g a day. That's basically two eggs.
So imagine the child that you see here waking up in the morning, either they or their parent is making them a couple of eggs, and that's all the protein that they're going to be able to eat for the rest of the day. And so that's what a patient or a parent has to live with. And so ideally, they can be able to fundamentally change that. Now, if they were trying to control, again, how much protein, they have to take this, if you will, chalky, really smelly shake that they have to do in order to keep that protein down. Because if they don't, that particular eventually what causes the disease is going to be able to go and cause those seizures that really fundamentally change the way that the patients have to live.
So our goal is to be able to provide a therapy that potentially allows them to, at the end of the day, be able to free them from all of these restrictions and allow them to live a more normal diet. Now, there are at least 60,000 individuals in the key geographies that have the therapy or, I'm sorry, that have PKU. And most of the patients you can see from this pie chart are not being able to be addressed and be able to change the way that they live their lives and be free from those restrictions and allow them to have a more normal diet. Now, the most efficacious therapy is called an enzyme substitution therapy.
Now, it benefits, but not all the patients are able to stay on it, as you can see here, partially because it does have a box warning, which there are individuals that can have a severe anaphylactic sort of reaction. The other issue is that some individuals develop an antibody or multiple antibodies to the therapy, really reducing the safety and the efficacy of an enzyme substitution therapy. And so there are other things, other oral therapies that are approved, but the way that that particular works is it relies on enzyme to be present in order to be able to be functioning. Our approach with MZE782 doesn't rely on the enzyme to be present and potentially can work across the entire spectrum on all of these patients and really fundamentally change the way that they live their lives.
Now, PKU is caused by, if you will, the toxic accumulation of an amino acid, phenylalanine, as it accumulates in the blood, and eventually, some of that particular amino acid, phenylalanine, gets into the brain, and that's really what's causing the seizures, and so what you can imagine, if you will, this idea that your body is a house with complex plumbing, moving around fluid and getting rid of waste and the toxins, and really the toxin becomes a sludge that really starts to accumulate in the blood, ultimately that needs to be removed. Now, substrate reduction therapy, as we call it, simply removes the sludge, allowing an individual to live a more healthy life.
If you see the graph here or the picture that you see here on the left, a person that has health or that's healthy basically has enough enzyme where they're able to remove the sludge from the blood. In the middle, unfortunately, a PKU patient, you can see the green dots accumulating in the blood. That sludge no longer can be removed, ultimately making its way into the brain. With the purple dot here, you see on the right with MZE782, by inhibiting the target, we basically get rid of the sludge by excreting it out into the urine.
And that's important because what we can do is start to measure that because we knew that going into our phase I, we can measure how much phenylalanine is accumulating in the urine and measuring how much we're being able to and eventually predict how efficacious this therapy could be for patients. So we want to be able to measure that phenylalanine in the urine, and we did that in our phase I. And we reported that data last fall with MZE782 showing that with strong results here. Just to orient you, on the left is our single ascending dose, but I want you to focus on the multiple ascending dose here on the right. And what you see here on the x-axis are all the doses that we explored in the study.
The y-axis is the amount of urine, the Phe that's accumulating in the urine, so the fold change. And we did that in the groupings you see here over three different periods. Now, in the literature, what was described, what you see in this dotted gray line in both of the graphs are really sort of the benchmark that we wanted to beat in this study. Previous literature had shown that there was at least a 10-fold increase in urinary Phe. And what we showed, as you can see on the graph, is exceeding 40-fold. All of our doses were able to do that. And again, we were able to exceed 40-fold, really being able to show for the first time not only this type of mechanism and the promise that this could be a best-in-class molecule.
Now, based off this data, we're expected to initiate our PKU phase II. We've talked to a lot of key opinion leaders about this. There's tremendous excitement about this particular data that you see here. It can fundamentally change the way that patients can live their lives, and so based off of that, we're rapidly moving forward with starting our phase II by the middle of 2026. Now, we're also advancing MZE782 in chronic kidney disease. 37 million people in the United States have chronic kidney disease. There's been no precision approaches, and what we're trying to do with MZE782 is be one of the first programs that really uses genetics in a way to better understand the disease, and based off the data we had last year, we are on track to start phase II in the second half of 2026.
Now, if you talk to a kidney physician, what we know is that they are working very hard to try to keep patients out of dialysis. At the end of the day, they want more medicines or more options to treat patients because there hasn't been a lot of innovations or new medicines that keep their patients out of dialysis. Because once they enter into dialysis, what physicians know is that their 10-year survival is very horrible. It ends up being very similar to a metastatic breast cancer patient. Now, there are a few new therapies that are out there, including a new class of therapies called SGLT2s that have become an important and vital part of how kidney disease patients are treated today. Unfortunately, not all patients are benefiting. One in four individuals are not really being able to change their kidney health based off the therapy.
And we know the one-year, if you will, discontinuation rates are very high, over 40%, and in part because of the complications that arise by being able to take the medicine, including hypoglycemia or low blood sugar or urinary tract infections, which sound very benign, but for elderly population, there are individuals that have so much of this to get this what's called a brain fog, ultimately forcing them to come off the therapy. With MZE782, what we have is an opportunity to complement SGLT2s or maybe even replace SGLT2s for patients who might be better suited for this. And our goal, of course, is to be able to develop that. Now, last year at the seminal kidney conference called ASN, we showed in vivo proof-of-concept, preclinical in vivo proof-of-concept for the very first time. Our scientists generated not just the molecule, but the data that you see here.
Tremendous excitement from the overall community as we were the first group to do that. Now, in order to orient you on the slide here on the left, that's UACR. UACR, again, is this idea of how much protein is measured in your urine. You want to just see that decrease over time. And what we have here on the x-axis are all the different agents that were explored. In the green is our compound. In orange is an SGLT2 inhibitor. And the black column are basically the combination of. You can see our agent be able to dramatically reduce UACR or the protein in the urine, do it better than the SGLT2. And what's nice to see is that together, you can see this additive effect such that it's basically getting to a normal state.
Now, we also measured different markers as well in terms of injury of the kidney, including what's called KIM-1 you see here in the middle. The x-axis is the same in terms of the agents. In this case, it's the different marker, KIM-1, and the amounts. Same type of trend here in the sense of being able to reduce it, do it better than the SGLT2, and together, you can see that type of additive effect that allows us to give us the confidence based off of this data, previous genetic analysis that we've done to really be able to advance this into clinical development.
Now, it's important to note that going into the study, we knew that based off of talking to nephrologists as well as our own review of the literature, that all approved kidney disease medicines or most kidney disease medicines showed this phenomenon of what's called an initial eGFR dip. Now, eGFR is basically a measurement of your filtration of your kidney health, so in this case, you want the number to be higher. The higher the number of eGFR, the better that your kidney is at filtering out the toxins and the waste. Now, what we wanted to be able to do because we knew that the fact that all approved agents had shown this type of initial effect, we wanted to look at it in our own study, and what you can see here on the left is the example of an SGLT2 inhibitor.
And it's a little bit counterintuitive because you see this initial eGFR dip. But because I just told you, you want to see this number as high as possible. But that actually is indicative of long-term renal protection. And what you see here over time is a slower rate of decline relative to placebo. So ultimately, what this graph is showing you here is that the people on the SGLT2s, statistically significant, were healthier in terms of their kidneys relative to placebo. Now, this is important because if we can see this type of initial eGFR dip, even in our healthy volunteer study, that would indicate for the first time clinical proof of mechanism that we could have an agent that for the first time is potentially a new class of therapies that could ultimately complement or maybe even replace people on SGLT2 inhibitors. And we saw exactly that.
In our phase I data that we reported, not only in the fall, but with subsequent data that we showed at the seminal k idney conference at ASN last year, we showed two things, and on the left, what you see here at the x-axis are the exposures of the different doses that we took into the study. On the y-axis, you see eGFR change, and you want to see that initial dip. What that graph basically shows you is that you see this dose-response relationship. On the right, you could double-click on one particular dose that we wanted to pay attention to. On the x-axis this time, this is the time, and the y-axis is the eGFR, and you can see that initial dip. Two things to highlight on this graph.
Number one is that we know it's due to the treatment because you can see that at the top of that graph, when we take them off the treatment, it bounces back up. So the eGFR does bounce back from that initial dip. And the orange line that you see here, it really represents SGLT2, and we can see that our particular agent has a dip that's similar, if you will, to the SGLT2 inhibitor. So not only do you see one, a dose-response relationship. Number two, we know it's due to the treatment because when we take them off, the eGFR bounces back. And third, this is in the range of an SGLT2 inhibitor, really indicating that this could have long-term renal protection. Now, we showed this data to kidney specialists and kidney physicians at the conference. Tremendous excitement about the ability to have and explore a new mechanism.
And based off of that particular feedback, we're designing our phase II, and we'll give more insight onto that later in the year, but we're poised to start that particular study the second half of 2026. At Maze, our vision is to build the next-generation precision medicines company where we're taking genetics and translating them as best as possible to build best-in-class medicines for patients primarily in kidney and metabolic disease. Number one, we have the pipeline with near-term catalysts that allow us to really be able to demonstrate value for patients. The second thing is that we've really been able to develop a differentiated platform and technique that allows us to think about additional programs that we can carry forward using our advanced genetic techniques, applying that to develop precision medicines for patients in kidney as well as metabolic diseases.
We also have the team and the capabilities to execute it on the milestones that we described today. And more importantly, we have the capital to be able to do this based off of what we've been able to accomplish from a financing standpoint, as well as our partnership. We have the operating capital to support all of the particular milestones that I described into 2028. And that really allows us, if you will, to be able to develop our medicines going forward. Now, the last thing I'd probably like to say is, before we go into the Q&A, a couple of things. One, we look forward to giving you the update on our progress, in particular Q1, later this quarter, when we were able to talk about our top-line proof-of-concept data.
And the second thing I do before we go into Q&A is really take this as an opportunity to recognize our team at Maze Therapeutics, who are working so hard for the patients that we try to serve and being able to work, if you will, being able to advance these medicines for patients. And with that, thank you.
Thanks. Thank you, Jason. So I'm going to kick off the Q&A, but there will be an opportunity for people in the audience to also ask a question. I'm going to ask you, because I'm going to get asked a million times, if you could give me any more granular timelines on when the MZE829 data will be. I know you said 1 Q, but February, March. Yeah.
To reiterate the guidance, we said at our last earnings that we would do this by the end of the quarter.
We're going to maintain that guidance.
And then I know you talked about the population that you're going to be studying. Broad AMKD focused on diabetes, not diabetes. Maybe you could talk a little bit about the number of patients and the follow-up that we're going to get?
Yeah. The order of magnitude of what's been reported in the literature before, our goal is to show at least a significant and clinically meaningful reduction in UACR, at least 30%. So the key messages for the investors here and listening on the webcast, we want to be able to try to show an effect in broad AMKD that's with or without diabetes that hasn't been done before. We want to see at least a 30% reduction in that UACR number.
If we can do that Anupam , the idea is that we are able to start initiating our planning for phase II B/III, which could lead to an eventual approval.
Just to be clear, the scope of the data in terms of the amount of follow-up as well as the number of patients that we should be thinking about?
Oh, yeah. What's reported in the literature before was describing around 20 patients or less. We'll be in that same magnitude. That really gives us the confidence to be able to look at that particular data, think about how much UACR is being reduced. If we see that signal on both of these, both with or without diabetes, that gives us at that 30% reduction number.
That really allows us to really think about initiating planning for a phase IIB/III, because that would be the first time anyone has shown clinical proof-of-concept in that patient population.
And just to be clear, you're going to be presenting the proteinuria decline as an average change versus a categorical type of analysis or both?
Oh, our goal is to ideally show both, which is looking at the overall average of UACR in addition to looking at categorical analysis that really gives an understanding of how much UACR is being reduced in each of the patients.
And then just following up on your comments, Jason, you said these data will help inform what a phase IIB/III type trial looks like. But where does the FSGS cohort that you have in the study fit into all of this?
Yeah.
So just to clarify, within the non-diabetic patient population, there are FSGS patients that are allowed to be enrolled. We do have, for those in the room or on the webcast that are not as familiar with our HORIZON study, we do have a third cohort that has highly proteinuric FSGS patients, which is closer to what's been reported in the literature before. We haven't provided guidance on that particular readout. We really want people to focus, first of all, on the first readout, which is really about broad AMKD and showing clinical proof-of-concept. And then we'll provide further guidance on that cohort after the readout.
Questions from the audience? Feel free to raise your hand. Yep.
So just curious, does it impact in any way the hydrolysis capability of the kidney?
Sorry.
Hydrolysis impact on the kidney?
Yeah.
So if we go back to the mechanism again, what you can really see, and I have a good, better understanding of over time, is this is really more about how the podocyte or the kidney cell is being affected and causing that cellular damage, which ultimately, there's those two principles, right? One is that you can see basically that expression or overexpression of APOL1 in the podocyte that ultimately gets expressed into the cell membrane. And that's really causing those holes to be formed in the particular, if you will, podocyte. And then ultimately, what you get is that really influx of cations into the cell, causing overall cell death and damage, right? So it's more about that as a sense of what we're looking for in terms of that.
And what's nice about MZE829 that we know now is that it not only blocks the pore itself, which is important, so you don't have those cations influx happening, but we also know that it's working upstream and really being able to disrupt the assembly of the pore from forming to begin with. And that's important because of things like we know a lot more about APOL1 and how much it turns over in the cell. We know that the literature reports less than an hour that APOL1 is turning over, sometimes even 40 minutes. And so the idea that you're disrupting the assembly of the pore becomes important. You could end up trying to block all those particular pores, but if they keep reforming, that doesn't do anything, right? You want to be able to try to disrupt that.
Question from the audience?
Maybe switching gears a little bit, Jason, to the other program, the MZE782 program. I actually just have a broader strategic question, right? PKU, CKD, very different indications in terms of population size. And when you're thinking about developing a single product in a rare disease and such a massive disease like CKD, there are pricing considerations. So strategically, you're running both options, but where do we land ultimately?
Yeah. Thanks for that question on the MZE782. I think it reinforces what we're trying to do, as I described, the cadence and the sequence of our studies. Sequence matters in this case. So the rare disease, in this case, PKU, being the first study that we start, ideally that has a very clear registrational path for those that are in the room and on the webcast unfamiliar with it.
The amount of Phe in the plasma is the approvable endpoint, and the number of the people that get reduced that is also important. So the fact that we have a very clear line of sight of how much Phe we might be able to not only excrete into the urine, but ultimately reduce into the plasma becomes important. So what we want to be able to do is start that study as soon as possible because commercially, as you're pointing out, these are very different. Sequence will matter. The other thing to kind of think about is looking at different ways that you can have different product configurations. So one of the ideas, of course, could be looking at different formulation technologies or formulation techniques that allows us to have different products.
We will also be seeing and looking and examining the changing reimbursement landscape that is occurring today, which is some geographies are looking at indication-based pricing, some others are looking at value-based pricing. And I think we can look at different ways that we might be able to develop this. But most importantly for investors to understand right now on a JPM is the fact that sequence matters. The PKU program will go first, and that will really help sort of set the standard in terms of how to think about pricing.
Questions from the audience? Maybe just quickly on your cash position, which you said is into 2028. What key milestones are funded in there beyond the 1Q update for MZE829?
Yeah.
So what's great, based off the financings that we've accomplished, plus the partnership, what we have the ability to do is execute on the studies that I described. So not only do we have the ability to report out the data from the HORIZON study, we also have the ability to think about starting and completing the PKU proof-of-concept, as well as being able to deliver data as well on the CKD program, and be able to potentially, if we see the data we hope to see at the end of this quarter, initiate and start phase IIB/III study.
Any final questions from the audience? All right. Thank you, Jason.
All right.