Okay. So thanks so much for having. One second, sorry, we'll just let the room populate, and then we can go ahead. Are you introducing? Yeah. Okay. Right. Good afternoon, everyone. Today we have the pleasure of having Atara Biotherapeutics with us, and we have Jason, the Head of Communications and IR, with us today. We have about 30 minutes, including the Q&A and the presentation. I would like to request everybody, if you have any questions, you submit them at the bottom of your screen at the Q&A function. With that, I will hand it over to you, Jason. Okay, great. Thank you so much, and thanks for having Atara here today, to talk through how we're working to unleash the promise of cell therapy for both cancer and autoimmune diseases. Just getting through the standard FLS here. So I want to take a few minutes to kind of provide an overview of the company. So we're a leading allogeneic T-cell therapy company, and, I believe we can say that we're leading 'cause we're actually the first and only to receive a regulatory approval of an allogeneic T-cell therapy, and that is actually being currently commercialized, in Europe, and I'll get back to that in a second. But our platform is based on a very natural immune response to a very common virus called Epstein-Barr virus. Many of you will be familiar with this, otherwise known as mononucleosis, mono, kissing disease. 95% of us are infected by the age of 40. What we can actually do is take these cells from healthy donors that had this immune response to this virus, take the cells out, manufacture them, and essentially bank them as inventory. So why this is very unique and different from autologous, which is what all the current CAR T therapies are based off of, is that they're readily available for when a patient needs it immediately. We can get them, and we've demonstrated to get these cells to patients within three days. So the basis of the platform then is these T-cells are able to recognize Epstein-Barr virus. For diseases that are Epstein-Barr virus driven, such as an ultra-rare lymphoma, which is the basis of the first approval of this T-cell therapy called Ebvallo. Or we can take these same cells and put a chimeric antigen receptor in them, and then direct them towards a different target. And so for tab-cel, as I said, that's approved, and that's actually partnered out, and I'll get back into that a little bit later in the presentation. But for our CAR T portfolio, we have two assets called ATA3219 and ATA3431. And 3219 are two different kind of categories here. One is in oncology, and so that's for non-Hodgkin's lymphoma. We're expecting actually first data in Q1 of 2025 for that. And then for 3219 in the autoimmune side, is that we have one phase I study that we're anticipating to initiate end of this year in Q4, that has two cohorts. One is in lupus nephritis with lymphodepletion, and then one is in severe lupus, severe SLE without lymphodepletion, which would be highly differentiating. This is a cohort of patients that would otherwise really not be exposed to lymphodepletion. So to have an allogeneic outpatient administered therapy that also requires no lymphodepletion would be very differentiated. And And to the best of my knowledge, we're actually the only ones that are pursuing both of these cohorts in parallel, including the no LD one. And then finally, and I'll finish this a little bit later in the presentation, is ATA3431. This is actually a dual-targeted chimeric antigen receptor against CD19 and CD20. Which, like I said, I'll talk a little bit more about, but the IND is slated for second half of next year. So just to provide a little bit of context here before we kinda get into this, just for those of you who may not be as familiar. So autologous is what, like I said, all the current approved CAR Ts are. And what that means is that you take cells out of a patient, you manufacture them, you put the CAR in, then you return them. And now the challenge with that is that this can actually take quite some time, on the order of the fastest being a couple of weeks, the longest taking upwards of four, five, six weeks. And that can be extremely problematic for our patients, especially in the oncology space, that are progressing rapidly. You certainly don't want them to have to take four, five, six weeks and wait for this CAR T treatment where they may progress, they may need bridging therapy, and that's, that's obviously not ideal. Also, these cells are, of course, taken from patients that have had, you know, exposure to multiple lines of other therapies, chemotherapies that can have challenges from a genomic integrity perspective. These are just sicker cells. And then, you know, finally, the kind of a main limitation here is capacity constraints. So even in the best-case scenario, you know, the leading company in the CAR T space is only able to treat about 6,000 patients per year. Obviously, this is very challenging when you start talking about autoimmune conditions, when you're looking at hundreds of thousands, millions of patients. The scalability for autologous is impossible. It just... When again, you have one patient, you know, one therapy, one, one lot, one patient, or one dose. So it just, you can't scale this, and it becomes an economical impossibility, especially with very high COGS. Now, conversely, allogeneic is actually where we take these cells from healthy donors, and we're able to manufacture these, and then, like I said, store them. And so what's nice about this is that these cells are, heavily, you know, QC'd. They're from healthy donors. They don't have the same level of exposure, of course, to chemotherapy, any other, any other agents. And again, they're stored in advance of patient needs, so there's no waiting period outside of a couple of days for shipment. Now, what Atara does is we take, again, these healthy donor cells. So these are, again, patients that have been exposed and infected with Epstein-Barr virus. They produce these T-cells. We're able to essentially extract and enrich these, and we're able to use these as one part of the portfolio. Again, this is tabelecleucel, so this is for Epstein-Barr virus-driven conditions, such as post-transplant lymphoproliferative disorder, which is what it's currently approved for in Europe. In which we also actually just received our BLA acceptance a few weeks ago, with priority review and a PDUFA target action date of January fifteenth. So that program is moving along nicely in the U.S. But important here is what this platform solves for, and all allogeneic companies have to solve for this one kind of main conundrum, allogeneic conundrum, if you will. How do you get these cells in a patient without the cells causing an immunogenicity issue, or having the patient themselves reject these, these cells, so, like, host-mediated rejection? So the very elegant solution where pretty much everyone else in the, in the field gene edits the T cell receptor out, or they and/or they gene edit the MHC or HLA out, but we don't actually have to do that just by nature of it being an Epstein-Barr virus T cell, where the T cell receptor can only bind Epstein-Barr virus, you know, virus-based proteins. What I like to think about here is just to think like a horse without blinders. It can look left, it can look right, graze here and there, but if you put blinders on a horse, it can only look forward or straight. It's a very similar concept with Epstein-Barr virus T-cell receptor. It It only looks for those Epstein-Barr virus proteins. So if you stick them in a patient, it's not gonna go off and target all sorts of things, causing graft-versus-host disease. It only look at Epstein-Barr virus. And in fact, we've seen this across 600 patients, and this is the most, to our knowledge, of any allogeneic company that's actually used to treat patients. While we have not seen graft-versus-host disease as related to the product, so it's a very clean, safe profile for the Epstein-Barr virus T-cell platform. Now, the other part of this is: How do you get these cells in the body without them being rejected? So how we do that is actually just basic transplant biology. So if you think about an organ, you can't just stick any old organ into a patient that needs it. It'll get rejected, right? So you have to match it. So we do something very similar. It's called partial HLA matching, and so we have this degree of similarity that we do between our cell type and the patient. And again, we're able to have these cells persist for long periods of time, and we've demonstrated this through tabelecleucel, where we don't really get that host-mediated rejection because of that partial HLA matching. So again, what we do is we take these, you know, kind of intrinsic benefits of this T cell that we know is similar as possible to the commercially approved alpha/beta T cells, and then we put a chimeric antigen receptor in there to redirect that to CD19 or CD19, CD20. Just to hit on a little bit here of kind of the other approaches out there, is that most require that they have to take out the T-cell receptor, and we just don't believe that that is beneficial to the cell. Obviously, T cells have a T-cell receptor for a reason. They're a key survival mechanism and for the health of the cell. So again, having that Epstein-Barr virus T-cell receptor in there really adds and contributes to the fitness of the cell, versus having to take out the T-cell receptor or having an invariant T-cell receptor. So again, it's very differentiated from other approaches out there, such as gamma delta and NK, or other allogeneic approaches that require this extensive gene editing to knock these receptors out, which again, gene editing can cause chromosomal challenges, inversions, you know, translocations, deletions, additions. Not to mention just the general manufacturing and efficiency, where some of the best gene editing is 60%. If you have to do two, three, four, five gene edits, it's, you know, serial 0.6 times 0.6 times 0.6. So again, at the end of the day, your yield is extremely, extremely small. Now, what is kind of the ideal, kind of, a patient journey here is from an autologous perspective, what currently has to happen is that you have to, you know, sit down, you have to go into facility, you have to get apheresis, get the cells out, and then have it manufactured. Takes two, three, four, five, six weeks, as I talked about. You have to undergo lymphodepletion, and then you have to stay inpatient for potentially weeks, to monitor for very common side effects called cytokine release syndrome and neurotoxicity, called ICANS. Now, what we've shown with our own portfolio, with our own products, tabelecleucel, as well as another drug called ATA188 that we had in the pipeline, that's the same similar concept based off of Epstein-Barr virus T cells, but that was for progressive multiple sclerosis, is that we're able to show that this is off the shelf. These patients required no patient apheresis, so this is over 600 patients at this point. No lymphodepletion whatsoever. So we've actually been one of the few, if only ones, that show that our platform can be used as cells do persist, do expand without lymphodepletion. We only required a five to 10-minute IV and a one to two-hour monitoring. This is all outpatient. So again, we have to prove this in the clinic for the CAR T side of the portfolio, but this is really what we're aspiring to, especially in that one cohort with that lymphodepletion, is not having the patients have to be apheresis, no lymphodepletion, and a very, you know, quick outpatient, you know, easy to do, an infusion, which is vastly different than the current profile for CAR T. Now, beyond our core platform, talked about the Epstein-Barr virus T cell platform, we did engineer other, some other key features with this, and I'll just really focus on two of these. This is called the 1XX costimulatory domain, as well as the less differentiated phenotype. And so I'll just direct your attention to number four on the bottom here. So this is, again, we're taking this Epstein-Barr virus T cell. We still retain the TCR, the T cell receptor, as well as the HLA, as I talked about. But this CAR is ultimately what binds CD19, and this is what essentially how the efficacy is accomplished here, is it binds CD19. Now, what happens is that you can actually have too much of a good thing. You can have that CAR bind, activate, and it releases a ton of cytokines, granzymes, perforins, et cetera, and that can really cause this really fast peak proliferation and response. But the downside to that is actually these cells are almost, like, too activated. It's like giving a like, a kid too much sugar, and then they get really tired and sleepy. Cells do the same thing. And the other part of that is if you actually have too much cytokines released, and so you kinda have these negative side effects called cytokine release syndrome and that neurotoxicity that I was talking about. And so how we can get around that is basically is attenuating this activation to some degree. So you have a little bit softer of an up curve, but a longer tail. So you still have the same area under the curve, you know, the same activation and efficacy ultimately, but it's a little bit shallower of a curve, so you get a little bit less of that kind of cytokine burst to begin with. And that has translated, and we'll show this in the next slide, clinically to less CRS, less ICANS, as well as really high efficacy. Because again, these cells don't kind of senesce or exhaust. And then the other part of this is a less differentiated phenotype. The way to think about this is that cells can kinda take different states. One is what we call an effector phenotype. This is a cell that's kind of like the soldier, goes out and does its thing. It binds the cells, kills the cells. But ultimately, they can't really make more of themselves 'cause they're completely differentiated. On the other side is more of a stem-like phenotype. They can make a lot more of themselves, but they're not really in that right phenotype to go out and kill cells yet. So ideally, you kinda want something right in the middle. So this is really where we've, you know, figured out and tinkered with, is to get that central memory phenotype, and it's like this really nice kind of hybrid between cells that can differentiate in the body to the effector cell type and, you know, need to do what it's doing, but can make more of itself for that kinda long-term serial killing. So again, we've kind of combined all of these into one platform, one cell type, that's ATA3219. And I think important to focus on here is that each one of these components has been clinically validated. So talked about tabelecleucel in ATA188. That platform has been used in over 600 patients. Our friends at Memorial Sloan Kettering actually used an earlier version of tabelecleucel, so that EBV CAR-T, or that EBV platform, put a CD19 CAR-T in there and actually showed overall survival up to three years in this post-transplant B-cell malignancy patient population. It's a really good long-term efficacy, and this does not include that 1XX costim domain or memory phenotype. YTB323, this is Novartis's asset. This is essentially Kymriah 2.0, the only difference being is a less differentiated phenotype. And by again, just switching that phenotype, you can appreciate, and I'll really call this out here, is that they use 12.5 million cells for DL2 and achieving a 73% CR and 62% durable CR at six months. That's just changing that phenotype, and that potency is drastically increased. So again, less cells, less, you know, chance of having CRS and ICANS and drastically higher potency, so that's great. And then TAK-940's Takeda's asset that they did in oncology. They've since discontinued it, but they had 1XX costimulatory domain in there. And again, if you look at the 25 million DL1, that's, you know, 10x less than the corresponding autologous, and, and Novartis was 20x less, and still getting 87% ORR, 75% CR, again, with a really, really good safety, safety profile. Now, for the NHL opportunity, I'll just go into a little bit of background here of... There's, you know, there's still a very high unmet need, actually, despite having so many CAR-Ts, autologous CAR-Ts in the space, that again, because of that side effect profile that you see in CAR-T, the CRS, ICANS, it does require monitoring your lymphodepletion. So it really kinda concentrates us in these kinda tier one academic centers, where, as we know, a lot of the patients, at least in the U.S., are not within the proximity of these large academic centers to receive CAR-T. So as a result, only 20%-40% of eligible patients actually receive CAR-T therapy, and the other part of this also is capacity constraints. There just literally aren't enough manufacturing slots from an auto perspective. And there's also durability challenges. Certainly in the third line, the B cell, which we're looking at, is that only 30%-40% are actually having durable responses at six months. So there's a lot of opportunity to come in with an allogeneic approach, be able to have, you know, expand this into community centers and really increase the, increase the access to this, and then hopefully have a better efficacy profile due to the memory phenotype in, in 1XX costimulatory domain. And then also the bispecifics, of course, are out there, still a challenging safety profile, and they have limited, you know, other challenges, including limited tissue penetration, require, you know, repeated administrations, because of the, the low durability. And then the other allogeneic approaches out there really haven't solved for this challenge yet. There's still durability and persistence challenges that are still happening. So what we saw or what we've seen in the preclinical side of things is looking at a very challenging Nalm-6 model for CD19 positive tumor model, is that we already see a much longer persistence versus the auto CD19 benchmark. And how this essentially is set up is we take the same donor cells, and we bring it through two different kind of manufacturing pathways. One essentially produces autologous CAR-T, one produces our allogeneic CAR-T CD19. So you're really comparing like with like, allo versus auto, and we're seeing much longer persistence as well as superior efficacy. It's notable that, you know, you see most people, most companies only presenting this up to 30, 40 days. We're actually able to looking at 50, 60 days in this model, which is really, really unheard of. It's really challenging to see it go out this far. So again, preclinically, it looks really interesting. Now, shifting gears a little bit to the autoimmune side, I wanna just highlight a little bit of kinda the background here is, I think most may have seen Dr. Schett's data that came out mid last year that really kinda galvanized the field of, you know, taking the oncology CAR-Ts and moving them into the autoimmune space. It's since been published in New England Journal of Medicine, and the field has just exploded from here with CAR-Ts and pretty much every autoimmune indication now. But he initially came out with a study, academic study, and 100% of the patients that were receiving the CAR-T therapy attained long-term drug-free remission, which is just incredible for these patients, incredible efficacy. And it's since been largely recapitulated across industry data, mostly coming from EULAR a couple months ago. There's an extremely high unmet need in a lot of these autoimmune conditions. A lot of them don't have any approved therapies. There's a lot of off-label things that just don't work that well, and there's just significant scalability limitations also from autologous CAR-T side, as I talked about. When you're looking at these large indications, they just can't get there. And then lymphodepletion-free approaches are really needed to minimize toxicities. There's a lot of logistical complications with this. I don't think people appreciate either that you have to really have a, you know, a hematologist, hemonc, closely connected with the treating physician on the autoimmune side, whether it's a rheumatologist or, or what have you. And so to coordinate all of that is also, you know, obviously just increased or incremental complexity. And then you're also looking at patients, again, a lot of autoimmune diseases skew more female. Females at, you know, reproductive ages, you know, don't obviously wanna be exposed to toxic chemotherapy, lymphodepletion regimens. So getting, you know, these CAR-Ts in that patient population without lymphodepletion is gonna be critical. So we're very excited about that. There's been very limited allogeneic CAR products with clinical data so far, so-... Really, everyone's kind of in the race together here, and a lot of data will be coming out, you know, end of this year and into next year. And so that, you know, really brings us to 3219, and how it's designed is we have that differentiated T cell platform that I talked about. It's allogeneic, so there's no apheresis. There's starting with healthy cells. It has that scale potential. And then also some preclinical data that we presented a few months ago, which I'll go into right now, demonstrated a really unique profile for 3219, that we actually saw the same level of B cell killing as the autologous comparator that we're doing, but a much reduced inflammatory cytokine profile. And what this may translate to, you probably see where this is going here, is less inflammatory cytokine release. Ultimately, we would think would lead to less cytokine release syndrome and/or ICANS. So obviously, we need to prove this in the clinic, of course, but preclinically, this looks extremely interesting that that 1XX costimulatory domain and memory phenotype, again, softening that activation curve, really does look like it's demonstrating a superior profile in preclinically, but still maintaining the efficacy. So again, that preclinical profile looks very interesting. I'm really excited to see what this does in the clinic. And then finally, as I alluded to, we are opening a new cohort in severe SLE later this year, concurrent with the lupus nephritis cohort. And we're really excited about this. As I talked about, we've treated over 600 patients across our platform without lymphodepletion, specifically in tabelecleucel. That, you know, we're looking at over 400 patients that we've treated with really good efficacy. Then obviously, this is the basis of our approval in Europe and the BLA that we filed and that we just got accepted. So, you know, we have data that basically demonstrate that we're able to, you know, put these cells in the body and due to the partial HLA match, you know, 1XX costimulatory domain, we're not getting that rejection that can, you know, hopefully allow us to remove lymphodepletion completely. So again, we're very excited to see what happens in this cohort. Now, finally, for the CAR-T side is our CD19/CD20 CAR-T program. Again, from an oncology perspective, cancer perspective, one of the key mechanisms of resistance and relapse is really selectional pressure in the microtumor environment. Tumors downregulate CD19, and so your CD19 antigen is no longer there, so the therapy no longer works, and that's, you know, hypothesized to be a major cause of resistance or disease relapse after the CD19 CAR-T treatment. So again, looking at and targeting both of these would most likely cause or, or allow potential incremental efficacy, and we've already seen that across multiple companies. One of them in particular, CBMG, actually licensed their technology out to J&J last year for $245 million. So, you know, they had excellent efficacy. It was a 91% ORR, and it was, you know, 70%-80% CR. So, but again, that was autologous, and it wasn't optimized for a memory phenotype, nor did it have a 1XX costimulatory domain. So again, we're very excited to get this one into the clinic as well, and we're expecting an IND in the second half of 2025. And again, preclinically in a very challenging, for those that understand and know this well, that the Raji model is extremely challenging. It's a CD19-low, CD20 model. We're able to already show greater antitumor efficacy just with the tumor burden on the left here, much lower, and then just the% survival, again, is dramatically higher than the autologous counterpart. Now, just kind of finishing on the CAR-T or on the tabelecleucel side. So I just wanted to again orient everyone that we talked about 3219, both on oncology and autoimmune, and 3431. Tabelecleucel, like I said, is currently approved in Europe under the brand name Ebvallo. This is partnered out with a French-based company called Pierre Fabre, which when we actually expanded our partnership with them last year, so they have global rights to this, to this asset now. So just wanted to provide a little bit of the deal kinetics here, that we have up to $640 million potential consideration, and we've received $27 million at closing, $20 million at the DS-BLA filing, and we just received $20 million at BLA acceptance, and we are anticipating or expecting an additional $60 million at BLA approval. So again, we're—you know, it's a great partnership. This is kind of their beachhead product to get into the U.S. marketplace. So this is really what they're building their entire team around in the U.S. They're very excited about it, and we're excited with them. And just as I talked about, the BLA has been accepted with priority review with the PDUFA date of January 15th, 2025. So we're tracking towards that extremely well, with peak sales of $500 million estimated in the US. And then finally, I'll just conclude on that we have, you know, $35 million, as we just reported in our quarterly update. But I just wanted to just say that it did not include that $20 million that we just received from Pierre Fabre, nor the $15.5 million that we just sold intermediates to them as well. So we actually have a pro forma of about $73.2 million right now. We're very comfortable from a cash position that allows us to get to all of our milestones that I just outlined. So with that, I want to thank everyone for your time. Please reach out if there's any further questions or you wanna connect and have, you know, a little bit more of a deep dive on Atara or any anything specific, and happy to answer any questions. Thank you so much for your time, Jason, and thank you for the presentation. As a quick recap, can you just tell us what the main milestones are, and what are you looking forward for the next 12 months? Yeah, no, thanks for the question. So yeah, so you know, I, I think I'd start on the CAR-T side. So 32, 3219, our CD19 CAR-T. So again, we have the phase I study in lupus nephritis, as well as the severe SLE cohort with no lymphodepletion starting in Q4 of this year, with initial data to read out in mid 2025. And then our non-Hodgkin's lymphoma study has initiated its enrolling, and we're expecting initial data in Q1 of 2025. So I'd say those are the main data milestones, and as I just alluded to or talked about tab-cel is currently under review with the FDA, where it has a PDUFA date of January 15th, 2025. So that, you know, potentially it would be a major milestone for us in early 2025, and then, of course, the IND for 3431 a little bit later in the year. Right. Thank you so much. And for the new folks to the space, can you talk about the significance of autologous versus allogeneic CAR-T? Yeah, sure. No, thanks for the question. So yeah, so going back a little bit to the start of the presentation, so, you know, there's really two camps here, is autologous, is, again, where you take the cells from the patient. You, you basically send them off to the manufacturer, they manufacture, put the CAR, and then they bring it back. Versus allogeneic, 'cause where we actually have healthy donors that we have a very large pool of, we bring those cells in, we manufacture them, then we, and then we bank them with the... and they, and they're stored in inventory. So, you know, the biggest difference there is that the starting material for autologous is from a patient. So like I said, in oncology, those patients, oftentimes have been subjected to three, four, five, six lines of different therapies, chemotherapy, immunotherapies, et cetera, that can really actually damage those cells. And so oftentimes you'll have manufacturing failures 'cause the cells just aren't healthy enough, or there'll be some other kind of genetic defect that's very challenging and just a capacity constraint. As again, if you're talking about oncology, it's one thing, and even in multiple myeloma, we already know that you can't meet the demand right now. But in autoimmune, when you're talking about 8 million, 10 million patients across all the autoimmune conditions, you can quickly see that it is an impossibility for autologous to be a viable, and, you know, from an economical perspective and just scalability perspective. So that's really the beauty of allogeneic, is that you're able to take a donor, manufacture hundreds to thousands of doses per donor, and then bank them. So that way, that's really the way forward, you know, we believe, and a lot many believe in the allogeneic space, to treat those hundreds of thousands, millions of patients. So I'd say those are the major differences. And maybe one other thing to call out now in autoimmune as well is you can actually take out autoreactive T-cells from donors from an autologous perspective, which could be extremely problematic in autoimmune conditions, of course. So again, from a healthy donor perspective, you're able to pre-screen for those and essentially eliminate those to make sure that you're not re-injecting, or not just injecting autoreactive T-cells to worsen the condition. Right. Wow, that's pretty interesting. Can we just talk about cash for a couple of minute? I just read you recently reduced your workforce by 25%. Can you elaborate on how that impacts the portfolio cost savings, and how the funds will be relocated? Yeah, sure. No, thanks for the question. So yeah, we just released our quarterly earnings a few days ago. So we ended the quarter with about $35 million in cash, and as I was just talking about, it didn't include the $20 million milestone payment from Pierre Fabre that is in the bank as of last week, plus $15.5 million that we just sold in intermediates, plus a little bit from accounts receivable. So again, pro forma, it's putting us about $73.2 million. So we're in a very strong, you know, cash position, that actually along with, the $60 million anticipated from Pierre Fabre upon BLA approval, as well as, you know, the, the double-digit significant royalty stream that we'll have in commercial and sales milestones actually puts us in the cash, runway into 2027. So we have a nice long runway. Like I said, it gets us through the major milestones. And yes, to the question or the point that we did have, two reduction in forces, actually, one last November, one in January. Those have started to flow through from a savings perspective, and as we said, we were expecting a 35% year-over-year in OpEx decrease, due to not only the reduction in forces, but also shuttering one of our older programs in progressive MS. So you'll really start to see realization of that in this quarter and next quarter, where you'll see kind of a step down in cash burn. And then early next year, when we offload tab-cel completely to Pierre Fabre, you would expect another step down from cash burn, because of that. Right. So we're about to end with our presentation today, but if you have any final thoughts that you would want to leave the investors with, please take the stage. Yeah, no, again, just thanks, thanks for everyone's attention, and I would just call out that we have a very exciting next 12 months. The CAR-T portfolio is, well, really the only one in the industry that has the base platform supported by over 600 patients worth of data across other programs that we've had. That's super exciting. We're actually the only ones, like I said, pursuing this kind of dual cohort approach for autoimmune, that if we can get there with allogeneic approach and no lymphodepletion, would be incredibly differentiating for the field. And I think that most physicians and patients would greatly appreciate the simplicity and not being exposed to lymphodepletion. So again, please reach out with any further questions. I really thank everyone for their time. Thank you so much, Jason. Thank you for your time today. I hope you have a good time at the conference. Thank you. Thank you.