Good afternoon, everyone and thank you for joining me at the second day of the Needham Healthcare Conference. My name is Gil Blum, and I'm a Senior Biotech Analyst here at Needham & Company, and I cover the cell and gene therapy space. It is my pleasure to have with me today, Bob Valamehr, the President and CEO of Fate Therapeutics, as well as Kamal Adawi, the Chief Financial Officer of Fate. With that, Bob and Kamal, you have the stage. Go ahead.
Thank you, Gil, for the invitation. We're excited to be here. It's been a fantastic event, and we'll start with this presentation that I hope you can see. Kamal's here to help me if I need help. This is the forward-looking statement for your review. I thought I'd start off, Gil, with just talking about what's the power of CAR T cells, why this introduction of chimeric antigen receptor into a T-cell is so exciting and such a change in fundamental paradigm of treating patients. If you're not distracted by what's going on the right-hand side, you can look to the left.
I apologize, this is very kind of a childish cartoon, but it really gives you the perspective of what I want to talk about here is, when you have in the upper left-hand corner, when you have untreated disease, it expands, it persists, and it continues. Conventional drugs, as you see in the lower left, have an effect. They're given, and they do reduce disease burden, but they decay over time. And that decay eliminates the full potential of the medicine to either completely eliminate the disease or bring it down to a level where it's no longer detected, or a patient can live in remission. When that decay goes down to a minimum level, the disease comes back. CAR T being a living drug, and this is where now you see that film on the right-hand side, it actually expands based on the disease burden.
Depending on how much you put in, that is not the ultimate number of cells that are going to be fighting the disease. Depending on the burden of the disease, the CAR T expands, and that's a fundamental biology of T-cells. They expand upon antigen exposure. As you see in the cartoon or in the movie, those little black dots you see in the beginning are the CAR T-cells, and the larger number of cells in red are the tumor. Over time, I hope you can appreciate, without adding any more cells, the CAR Ts expand and thoroughly eliminate the disease. This is what we're all excited about and we're trying to bring to patients, whether it's in oncology, autoimmune disease, or other applications. I'm not going to go into this too much, but there is this value proposition with CAR T.
Not only what I showed you in terms of a living drug expanding and coming into a combat against the disease burden, but it also has other fundamental attributes that are better than traditional biologics. That includes trafficking and multiplexing the product to be able to go after complex diseases that are not just homogeneous and uniform. Most diseases, whether it's cancer or lupus, is very complex and heterogeneous. So, really CAR T gives you that ability to not only expand with the disease and overcome the disease through the drug product expansion, not only it can traffic into those places where the disease hides, but it also has the ability to be further edited so then it can go after complex diseases. This is a very exciting drug therapy that I hope is in everyone's hands in the near future.
There's also the other side of this. CAR T works, and some are doing in vivo. I think in vivo is a great idea, but it is not controlled. And because you have a product that expands and has this unique ability to really be aggressive, you want to have control all around it. You don't want to just go in and, through uncontrolled ways, introduce CAR into the body. You want to have it very controlled. So, I think we sit in the very middle of the sweet spot of potential for amazing therapy, but also controlled safety profile that comes with a traditional drug product that's been developed. How do we do this? How do we create a uniform CAR T that is accessible to all patients who need it? That starts with our stem cell population.
Our stem cells are engineered, and the reason we use these stem cells and engineer them is because they have this unique ability to grow. We can go down to a single cell and then expand that selected clone and make it into a master cell bank. We would have done this with T-cells, but T-cells cannot grow in this unlimited way. So we go to a stem cell population as the starting material. As you see here in this cartoon, we engineer the iPSCs, the stem cell population, as a pool, just like how T-cells are engineered as a pool.
Because we have the ability to take individual clones, we can then screen those clones and find the perfect clone that has all the desired attributes without the undesirable off-target engineering, take that clone, make it into a master cell bank, and then have the stem cell population be the starting material for every manufacturing batch so that we can make thousands, if not billions of doses and be able to treat all the patients who are in need of this. This gives you consistency, this gives you reproducibility, and this gives you lower cost of goods so then you can now have what we ultimately desire is accessibility for all. Great patient reach. Currently in our manufacturing facility, which is 40,000 sq ft, we are able to make thousands of doses.
This is very different than your traditional CAR T platform because one iPSC master cell bank, one of those stem cell master cell banks, can give you over 10 million doses. We will not be going back to the donor every single 1,000 doses manufactured and re-engineering a donor, whether it's the same donor as a previous CAR T product made or it's a different donor. We don't really go back. We just have the starting pool that we continuously access. So engineering is not repeated, um, s earch for comparability is not repeated. We essentially have a master cell bank that starts it all off. In our current facility, we can make 50,000 doses without really creating too much need for increasing capital equipment. Our facility can provide you that. This can be raised even higher with increase in volume or increase in size.
These numbers that I'm sharing with you 50,000 doses per year, is what we can accomplish today with just hiring more qualified manufacturing associates. This is less about needing to get more reagents. This is basically the process and it can be scaled. And because we have our manufacturing in-house and under control, we have great ability to make whatever we want here and not be limited by a third-party schedule or issue. This facility supports both U.S. and international clinical development. I hope you see that we're very different than your traditional CAR-T. So just to go back, CAR-T, I think, is an amazing product, but to make it is very challenging, it's complex, has a lot of steps to take, and a patient just doesn't go into the doctor's office, get prescribed, and have the medicine available to the with traditional CAR T.
I hope what I will show you in the next few slides is that we have now accomplished that, where we have the ability to give a patient on-demand CAR T cells in an outpatient setting, and that CAR T cell that's given is safe and effective. There is a lot of opportunity in terms of what we could do next, and I'll talk about that as well. Again, we sit in a very unique stage of the development of bringing CAR T cells to patients in a broad manner. Because we can engineer CAR T cells in many different ways, we have a pipeline that is very exciting and has multiple indications in mind. Mainly here we focus on autoimmunity and on oncology. Where I will focus mostly on is in autoimmunity with FT819.
This is a CAR T-cell that carries CD19 targeting strategy through a CAR. I'll also talk about FT839, a very complex 13-point edited CAR T-cell that you can essentially only make with this platform, and I'll show you why you should be excited about that. That's in an IND-enabling stage, while FT819 is in a phase I/II study. And in oncology, we have several products, including FT836, that uniquely targets an antigen that's in theory on all transformed cells. I'll talk more about what that means and how we're very excited about the early clinical data that we're seeing with FT836 that eliminates the need for conditioning, while at the same time going after solid tumors that have significant unmet need because current therapy is not working.
When you add all this up, there's a lot of patients that can be treated by these products and a lot of opportunity in terms of commercialization. We're very excited about this as well. FT819, this is an off-the-shelf anti-CD19 CAR T-cell product candidate, as I mentioned earlier. It is very uniquely made. It is made to balance safety and efficacy. We didn't want to go in and have in our first product, first CAR T product an uncontrolled product where expansion might be, in some situations, not ideal and resulting in toxicity that we do not want. This is a master cell bank, and we want the product to be safe and effective.
And so, we fine-tuned the CAR through collaboration with Michel Sadelain to knock out items two and three so that we end up with a CAR that can expand, that can promote antigen-mediated expansion, but in a controlled way. In addition to that, we put the CAR into the TRAC locus, where now we have biology that controls CAR expression, not a synthetic promoter that is overwhelming the cell with CAR expression. This allows FT819 to have these unique attributes and the efficacy of a CAR T but is controlled. And that is very important as we talk about when it comes to safety. So, this is really an exciting product that balances safety and efficacy.
When we went into the clinical trial, we thought about autoimmunity because, as was shown very nicely in early 2020s, 2021, 2022, is that targeting CD19 in lupus nephritis and SLE is an effective treatment strategy. We've known this before, but with CAR T cells, it was a unique angle. We started the clinical design with two approaches, Regimen A and Regimen B. Regimen A had three different conditioning arms, cyclophosphamide and fludarabine, which is being used by all CAR T companies. This conditioning allows the CAR T to expand. It is also a disease debulking agent. You get a lot of unique attributes when you combine conditioning with CAR T cells. Here, as I mentioned, we started with Cy/Flu, like everyone else.
Then bendamustine was introduced as a second option because, at the time, fludarabine had a shortage, and we wanted to make sure patients who were eligible were able to be treated. It's a less intensive conditioning than three days of Cy/Flu, but nonetheless, it's been shown to be effective in oncology. Lastly, cyclophosphamide, a single dose of cyclophosphamide, which we thought would be more aligned with how autoimmune patients are treated in general, because they do traditionally get either three or six rounds of cyclophosphamide during their treatment option. A patient who's excited about CAR T may not be concerned because cyclophosphamide is something they've been treated with before. Regimen A, to our surprise, only enrolled in the cyclophosphamide-alone or bendamustine-alone arms. When patients and physicians had the option, they did not pick Cy/Flu.
That's not a surprise, because three days of heavy, intense conditioning is pretty aggressive. I'll talk about our enrollment in a second, but I think this really helped our enrollment because we're giving an option for less intensive conditioning. In Regimen B, we hypothesized that maintenance therapy, it is suppressing the patient's endogenous immune system. Perhaps there's an opportunity for FT819 to synergize with maintenance therapy and be able to give the patient an opportunity to come off maintenance therapy because that synergy was able to reduce disease to a point where the patient can come off their maintenance therapy. It's a single dose of FT819 with either less intensive conditioning or no conditioning. As we started this campaign in 2023, we were having a hard time enrolling patients.
If you look at the lower right-hand side, you can see that the number of sites in gray and the number of patients in blue circles were limited in our first 18 months. That's because there are a lot of companies that were already in the field, such as Novartis and BMS, pharmaceutical companies with good reputation, or companies like Cabaletta that were established in this field. It took us a while to start enrolling patients. That's because I don't think many sites fully understood how challenging auto CAR T is in terms of product availability and patient desire to go through the process of having been treated with CAR T. Not only you got to come in early and procure your T-cells and come off your medication with no medication available to you right after you coming off your medication.
The other problem is once you're treated, you're in the hospital for extended period of time because of the safety issues that are seen with auto CAR T. For us, as we talked about being off the shelf, as we talked about our safety consideration, we really needed to have the sites experience that, the rheumatologists experience that auto CAR T challenge before they came back and appreciate who we are. And that's okay, because experience is more important than anything else. When we started going to conferences, showing our data, albeit with few patients, but also showing our process, our engagement with the sites really escalated and patient enrollment, as you can see in the past six months-nine months, has really advanced.
This is because the sites are appreciating, the patients are appreciating, the physicians are appreciating our ability to be on demand, the outpatient availability, so patient can be treated same day and discharged on that day. And also, as I mentioned, the safety profile and the efficacy profile. We're now global, as you can see, many sites in U.S. and outside of U.S., and also good patient enrollment. The patients are real-world patients, as you can see here, with multiple lines of therapy, previous therapy and multiple years with that disease. The data we'll talk about, it's not naive or a hand-selected patient population. It's about the real-world population receiving FT819 with less intensive conditioning.
That is an exciting part because as I talk about the data that's within the same ballpark as auto CAR T, when you look at the other attributes, such as less intensive conditioning, on-demand availability, cost of goods, you really get excited about this opportunity as we present here. Safety profile, as I mentioned, looks great. No grade three or higher CRS, ICANS, or GVHD have been seen as of the data cutoff. Really here, the top row shows you the drop in disease burden in different angles. One is the actual raw scores. SLEDAI is a composition of different disease manifestations. As you go from a number such as 20 down to four, you're actually reducing a lot of your symptoms, a lot of your disease categories.
We showed that by either actual numbers in the first plot on the top row or averages or means. You can get an idea how disease is coming down. In blue is dose level one, in orange is dose level two. You can see that not only there's a dose response, but the trend is actually pretty impressive in terms of how disease is dropping. Now, this is not unique to Fate. As I mentioned earlier, our CAR T is showing the same thing, but that's the excitement of CAR T. The top row just shows you how CAR T can drop disease in a very meaningful manner rather quickly. The bottom also shows you a different angle.
Another angle is I'll focus first on the lower right-hand side in terms of fatigue score as defined by FACIT or PGA, Physician Global Assessment. You can see that these patients very uniquely, I'll say, as I continue to ask our rheumatologists about this, you don't see this with mAbs or T-cell engagers. These patients are quickly feeling great. They're coming from a fatigue score or severe fatigue score, and within few months, they're out of their house. They're feeling great. You hear these testimonials time over time. This is not only reducing the disease inside the patient but also helping the patient gain their lives back. That's very exciting.
I am still looking for someone to tell me that, "No, you see this with steroids, or you see this with mAbs." To this date, no, I think this is very unique to CAR T-cells. Lastly, in the lower left side, that's the UPCR. That's one of the key indications of lupus nephritis and recovery from it is the score of your kidney function and how it's behaving. And this is for the most part, the angle we're going after. We want to look at complete renal response as a primary endpoint. I'll talk a little about our phase II activities. And so, here we're excited about not only reducing disease, not only improving patient lives, but also helping kidney recover. These patients can have meaningful lives after treatment.
This is more of a translational slide which shows that just like other CAR T-cells, FT819 is able to reduce the B-cell compartment by eliminating those B-cells and allowing for an immune reset or a rebalance where the new population that comes back is a population of more naive in nature, not a fully differentiated B-cell type. You see not just the disease change, patient health change, but also the B-cell compartment changing. In the right-hand side, it just shows that CAR T-cells, as I mentioned earlier, can go to different tissues and can migrate well and can eliminate B-cells in secondary and tertiary tissues, not just in blood, but in tissues where I think mAbs and T-cell engagers often have a hard time penetrating. In addition to SLE, we're treating patients in systemic sclerosis, vasculitis, and myositis.
Here is just a case study of a patient that was treated, a systemic sclerosis patient that was treated, and they also saw improvement in their health score. They saw improvement in their skin score. They saw improvement in their status, whether it's the Clinician Global Assessment or the Patient Global Assessment or the SHAQ. Everything is trending in the right direction. I think this is just the power of CAR T-cells. I show this because as we talk about the phase II in SLE, we are planning on additional phase II in other diseases, as I mentioned here, for example, systemic sclerosis. As we accumulate more patient data, we think we're on the right track to do more and not less. Where are we with FT819? As of the data cutoff of February, we've enrolled 15 lupus patients with just seven sites.
As I mentioned, we have 16 or so sites. This is February. We have more than this now, but you can see how powerful this on-demand availability is of a product that's desirable. Just with seven sites, we've treated 15 lupus patients. Our near-term steps is to complete the phase I SLE study and continue with the no-conditioning dose escalation, as I mentioned earlier. We have our RMAT designation for the SLE program with FT819. This allows us to have a lot of interactions with the FDA. They've been great with us over the past 10 years as we entered the CAR T landscape over the past 10 years. That conversation has continued. It's meaningful. We've had really good type B meetings, whether it's been on the clinical protocol side or on the CMC side.
Our next milestone is to pursue the phase II single-arm, potentially registration-enabling clinical study in lupus nephritis. It'll be a single-arm study, as I mentioned. We will be looking at complete renal response at six months as a primary endpoint, and the first focus will be on lupus nephritis, subsequently moving into extrarenal lupus. If the data continues to hold, systemic sclerosis would be an opportunity for the next phase II. Now, with that in mind, I wanted to shift over to our next-generation program. That includes autoimmunity and oncology.
As I mentioned earlier, because we have this unique ability to put a lot of engineering attributes into the pool of iPSCs and then clonally select the one that has all the desired attributes, this is a very busy slide, but it just says we have the unique ability to edit these cells in any manner we want. Today, we're focused on T-cells, but who knows? iPSCs can become any of the 200 cell types in the body. We're also in the background looking at other cell types, but today the focus is on engineering T-cells. We have a very unique way of avoiding the need for conditioning.
As I mentioned early on, conditioning brings in an element of creating space, avoiding rejection by the host in an allogeneic setting, and also reducing the disease burden. So, to really offset the need for conditioning, you got to come up with a powerful approach that doesn't just create a hiding situation for yourself. You want to have active stealth. You want to protect yourself from the host immune system and avoid the need for conditioning, but at the same time, you want to be able to expand. And this is where our strategy, our sword and shield strategy, becomes very unique. Now, there's a lot of science here, and I'll minimize it by just calling it sword and shield. But this is the best way to kind of give you the breadth of what this editing strategy does.
There's one side of it is an activated receptor that kills any activated immune cell that engages with you. 4-1BB is a very unique signaling cascade that comes in on effector cells late in their stage of killing the target. At first CD69 comes on, then CD25, then CD38. At the very end stage of engagement, 4-1BB comes up, and that's when the T and NK effector cell types begin to kill their host or their target. Here, before they can kill our product, our product will kill it, because it has an activating receptor targeting 4-1BB. It is very specific. It only kills a cell that's engaging with it because that's when 4-1BB turns on. You leave the other 99.999% of the T and NK cells alone.
You only target the ones that are interacting with you to kill you. Those that interact with you that don't want to kill you, they move on because they don't turn on 4-1BB. On the other side, we've knocked out CD58 to minimize adhesion. As I mentioned earlier, for a host immune cell to be able to recognize the product and kill it has to interact. By knocking out CD58, we actually minimize the interaction that the effector cell can have with our target. In this manner, we protect our product but allow it to expand as well. It really gives you all the advantages of conditioning, and that's been implemented in our next-generation platform. FT836, using that Sword & Shield technology, has nine edits. The main edit is the chimeric antigen receptor targeting MICA, MICB.
MICA, MICB are two stress antigens that are found on transformed and affected cells, found on senescing cells, found on fibrotic cells. They are the body's way of telling itself, "You got to get rid of me because I'm a bad actor." Obviously, as we know, cancer quickly evolves. What cancer and viruses have figured out is that by cleaving MICA and MICB, you avoid endogenous immune surveillance. What we've done is we've tried to be a little more clever than the virus and the cancer, and we actually go after targeting the region that's been left behind. That uncleaved region is what we can bind to with our CAR. Now we have this ubiquitous way of targeting cancer. It doesn't matter what the treatment was. We can now come in and be the first treatment of that line of therapy.
Because often when you come in and you're targeting, for example, antigen one and an ADC and a mAb have already targeted that antigen one, you're finding yourself in an antigen desert or clonal selection will prevent any unique ability that your product has to get rid of cancer. That's why cancer is so challenging. It evolves so quickly. Here, the way of our approach is the cancer hasn't figured out a way to overcome this targeting strategy, so we're very excited about it. Combining that targeting strategy with the Sword & Shield technology to avoid the need for conditioning and having other attributes sprinkled on FT836 really gives us a complete product for going after solid tumor, a disease that's very aggressive and very few solutions are available.
Again, this just highlights, you'll find on our corporate deck, the targeting strategy, the uniqueness, and the ubiquitousness of all these different cancers that fall into our realm of targeting. As you can see on the far right-hand side, where there is liquid or solid tumors, you can quite easily see that combination of MICA, MICB or both together, how 99% of these cell lines are all captured within that breadth of targeting capacity. We went in with a clinical design that basically had multiple arms. The two arms that we focused on was combining FT836 with either cetuximab or Herceptin, and that's because the CAR T-cells, in addition to having the CAR, have a CD16 Fc receptor that's been uniquely designed by us that maximizes the interaction with mAbs. Now we can target MICA, MICB, and EGFR or MICA, MICB and HER2.
We started with this clinical design, and remember again, no conditioning. What we saw was very exciting. In dose level one, first three patients treated, we saw that as you can see in the histology on the lower left-hand side, MICA, MICB is prominently expressed. When we give the patients FT836, we saw that without any conditioning, we could detect live cells in the blood. We could also, not highlighted here, but we also saw FT836 in the biopsy. It showed not only it was persisting, but it was trafficking.
One thing that we got very excited about, and this is early data, but at dose level one, we saw that a colorectal cancer patient that had five years of therapy without any major reduction in their disease burden. By day 29, we saw the cancer antigen biomarkers go down, and we got very excited because that correlate very well with tumor size reduction. By day 29, we saw CEA and LDH both come down over 50%. A month later, when we looked at the target lesions, we saw that they came down by 20%.
This was very exciting, not just a proof of concept, but a very exciting starting point for FT836, and that a CAR T that has this ubiquitous targeting strategy can go into a very challenging disease setting with really no unmet real treatment available and be able to reduce tumor volume. We're very excited about this. We're now at dose level 2, and we hope to give an update at ASCO. Again, very ubiquitous targeting strategy. Lastly, I'll talk about FT839. As I mentioned, 819 targets CD19, and that handles a lot of the autoimmune diseases that are B-cell focused, such as SLE. As we know, autoimmune and other diseases such as heme malignancies are very complex, and having a product that could go after more complex diseases would be highly sought after.
Here, not only we introduce a CAR targeting CD19, but also a CAR targeting CD38. We also introduced the Fc receptor CD16 to combine with mAbs, and also a CD3 fusion receptor to be able to combine this product with T-cell engagers. Because ultimately, we believe complex diseases require combinational strategy. This is for us for autoimmunity and for heme malignancies such as lymphoma and myeloma. This is the starting point for a combination strategy to go in. For example, you want to combine FT839 with daratumumab or other agents that are doing well in myeloma, then you can do that. Rituxan in lymphoma. This becomes now the synergistic point to combine CAR T with other strategies to have an effective outcome in eliminating disease.
Because of the Sword & Shield technology, it doesn't need conditioning, so it really gives you the ability to have good patient accessibility but also combination strategy. We're very excited about this. We're completing the IND-enabling activities and hope to treat patients in the second half of the year. As I mentioned, once you have this product, the disease indication opportunities are pretty large because those two targeting strategies, a lineage targeting strategy and a disease state CD38 targeting strategy, really gives you a comprehensive approach to targeting disease. The second half of this is essentially us moving forward in our oncology programs and next-generation autoimmune programs, and we hope to give updates as well on these events. I'll wrap it up, and Kamal is here to answer more in-depth questions about it.
We have good cash available to us right now. Basically, as we announced in our most recent earnings, we have over $200 million in cash. This is a result of reduction in operating expenses and so allows us to basically have cash runway through 2027. Thank you.
Thank you, Bob. The floor is open for questions, but maybe I'll start with a couple from us. Just looking at the SLE Regimen A data, you had at least one patient that showed basically disease recovery. I want to understand what kind of durability do you feel you would need from an off-the-shelf therapy in order for this to make a useful product?
Yeah, that's a great question. Right now, when you think about other off-the-shelf products, mAbs and T-cell engagers, they're given within the treatment cycle of first month multiple times, and they're given over a course of six months thereafter. For us, when we look at our availability and inventory, I feel that we can easily give every six months, and that would be a concept where one dose with conditioning, you come in every six months on Thursday, get the conditioning, come back Monday, get your 819, and leave. If we can maintain this type of response on FACIT and SLEDAI, and PGA, I think that is, compared to what is available today, a great advancement. For me, we have the availability and repeat dosing is not a sign of weakness, it's a sign of strength for us, and it's something that is being commonly utilized today.
As it relates to Regimen B, and this is my own observation, it didn't look like the B-cell aplasia was as strong as Regimen A. I know this is still probably too soon, but is there a regimen you're more leaning towards, or do you feel the data needs to evolve first?
No, absolutely. Today, phase II study is Regimen A. That's where we see the depth of response. Now with Regimen B, to be fair, we haven't really explored dose level two and the multi-dosing that the FDA has given us green light to pursue. At the same time, we have FT839. There is a little bit of a balance we got to do this year in understanding what's the best path forward with a no conditioning side. When it comes to our phase II study, we feel that FT819 with bendamustine, excuse me, at dose level two, is the ideal combination for effective and safe treatment.
I do want to spend at least a second on the endpoint that you mentioned prior as it relates to responses. You're going to have to focus on lupus nephritis. That's what that means, right? How challenging is this to enroll? I had a KOL a few months ago that basically said that if you try to enroll every study, you've run out of patients.
That might be true, but I think with the ease of this process, we might get the lion's share of those patients, if that makes sense. Right now, as our clinical trial is advancing in phase I, our enrollment is something that I no longer lose sleep over. We are treating patients, and we've gone from a dramatic not many patients to many patients. For me, a single-arm study can be completed in lupus nephritis in 12 months-18 months. We're targeting 12, but it could be as long as 18. I think it's quite achievable because it's a single-arm study. I think we'll get our share of lupus nephritis patients, maybe even more than our share.
Maybe you did mention this in the presentation, but just to focus our listeners, next data disclosure that you want people to pay attention to, and you've definitely increased the number of patients since we spoke last, but what do you think is a comprehensive update?
I think an update will be at EULAR. Probably the more comprehensive with durability update will be at ACR. Phase II will start somewhere in between those. Come ACR, I think will be the perfect storm of comprehensive data and appreciation of where the phase II is at. Not I think, I know. EULAR we will be presenting data. We have a couple of opportunities to present our data at EULAR. We're excited to showcase our data, including FT839 preclinical data as well.
Great. It'd be great to see you in London. Okay, I don't see additional questions from the audience, so I'd like to thank you for joining us today.
Thank you, Gil, for your time.