Good afternoon, everyone, and thank you for joining us on the third 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 actually my pleasure today to have with me Fred Aslan, the CEO of Artiva. Artiva is facing some truly interesting data coming up soon, and I think this should be a particularly interesting conversation to have. Maybe just to start off and set the stage, Fred, if you can discuss a bit Artiva, its technology, and your focus indication. Thanks, Gil. Thanks for having us at your conference. Artiva was founded in 2019 on the back of technology to massively scale NK cells that had been developed for a decade prior from a Korean company called GC Cell. Today, our lead asset is a non-genetically modified NK cell, which we combine with a monoclonal, and we can talk about the mechanism of action as we continue the discussion. We announced last year that we are prioritizing rheumatoid arthritis as our lead indication. We are focusing on rheumatoid arthritis because it plays to the strength of our product, which is the ability to potentially deliver a really deep B-cell depletion following on the steps of other work that has been shown in this space, but with a therapy that is actually quite tolerable to be used in a community setting and scalable enough such that thousands of people can actually have access to it at a COGS that is a lot more accessible and provides more flexibility when it comes to pricing. So, we're really excited. As you mentioned, we are approaching an important potential inflection for us. We guided that in this first half of the year, we would be sharing clinical efficacy data in RA in at least 15 patients, with most of those having six months or more of follow-up, as well as we will be providing an update on our interactions with FDA regarding a potential pivotal trial in this area. Well, maybe a good place to start is discuss AlloNK and more specifically, how do you view the attributes that make it a good potential product in rheumatoid arthritis? Yeah. So let's start with the mechanism of action, because I think it starts there. We are using non-genetically modified NK cells. That is pretty unique in the field. I don't think you are covering anybody else that utilizes non-genetically modified NK cells. There's a number of advantages for that, and we'll get into it. Because we don't genetically engineer our cells, and so there is a significant safety advantage, we have been treating our patients in the community setting from the get-go because we're not a genetically engineered cell. There's a number of tolerability items that you sort of embrace more easily when you're not genetically engineered. Because we're not genetically engineered and we're not engineering in a CAR, we utilize a monoclonal antibody to do the targeting for us. So we use rituximab as our partner monoclonal. Rituximab binds to the B cell, rituximab activates our NK cell, and our NK cells kill all the B cells. What we learned through this process, and we really learned this in oncology, is that our NK cells, in combination with rituximab, is able to drive a very deep B-cell depletion. In our oncology data, which we have shared over the last several years, we saw a complete response rate in line with auto CAR T and a durability which was also in line with auto CAR T. Today, we have patients that have been treated more than two years ago with aggressive NHL that continue to be in remission. And that is something actually quite spectacular because that has not been easily demonstrated with other modalities. We also utilized our NK cell in combination with a CD30-targeted biologic in Hodgkin's lymphoma, and again, we were able to demonstrate response rates and durability in line with auto CAR T. Because of this deep B-cell depletion, we figured we had the potential to actually develop a highly efficacious product that could drive a potential reset and durable clinical responses in patients with autoimmune disease. That's one piece of the story, which is the efficacy, right? We are going for a product that can be quite potent and quite efficacious. The second piece of it is the safety. What we noticed in our oncology experience is that we didn't have to hospitalize our patients unless there was a reason why the oncologist felt that the patient needed to be hospitalized for an infection or something like that. And so the vast majority of the patients that we have treated so far in autoimmunity have been in the community setting. What we're seeing is that despite the use of low doses of Cy and low doses of Flu, that our therapy is actually quite tolerable in the community setting. In November, we shared data on our first 32 autoimmunity patients, where we saw that there was basically only one patient that required hospitalization due to an ear infection, an ear abscess that had to be drained. They received IV antibiotics for two-three days, and then they went home, which is a very favorable outcome for our therapy, considering that we're trying to go for high efficacy, but with a tolerability profile that could be embraced in the community setting, where the vast majority of patients that we are going after actually reside. That all makes a lot of sense. One investor pushback that we hear as it relates to Artiva is that using Flu/Cy combined with rituximab is part of the treatment regimen in oncology. How do you show the contribution of the NK cell to drive responses and then not just be able to explain away everything with the conditioning regimen? Yep. So there are two pieces to your question. One is the response rates, and then the second is durability. Right? Maybe I'll go back to our oncology experience as we talked about earlier. When we were in oncology with our same regimen, rituximab, Cy/Flu, and our NK cells, and we had six months of follow-up in cancer patients. A lot of the KOLs that we presented our data to asked the question, but I can't really tell whether it's your NK cells doing something here or whether it's the Cy/Flu and the rituximab. Because rituximab is used in oncology and Cy/Flu is used as salvage chemotherapy. The same thing happened when we only had 12 months of follow-up. By the time we were getting more and more follow-up, it became unanimous from everybody that we show was like, look, this is definitely not the cyclophosphamide and the fludarabine or the rituximab that's driving these level of responses in patients that are so late-line. My expectation is that the same thing will happen in autoimmune disease. So cyclophosphamide and fludarabine, when they are used in the context of autoimmunity, because they have been, they're not very popular, but they have been used extensively. There's book chapters and a lot of papers from the late 1990s and earlier in the century where people talk about utilizing cyclophosphamide at least once a month, if not twice a month. Today, there's a Euro-Lupus dose of cyclophosphamide where you have to give it every two weeks. We're using doses of cyclophosphamide and fludarabine, which are a fraction of what were used in the past, and we're only giving it once before we actually give the NK cells and the monoclonal. So we would expect that perhaps the influence of Cy/Flu could be present in the first eight-12 weeks of treatment. By six months, it's very unlikely that at the doses that we're utilizing, that you'd see any lingering effects. The same thing is true with rituximab, though rituximab is given less often. So rituximab is usually given every six months, right? So what we hope to show people, and I don't think you need to actually wait very long to show this, is that we have very good data sets on rituximab. Rituximab was approved in 2006 in RA, for example. So it's almost 20 years of experience with rituximab. Hundreds of thousands of patients have been on it. If you show up with a dataset that clearly looks like you're doing something that rituximab would not have been able to do on its own, then you're making the case that it is the entire regimen that is actually driving the efficacy that you're seeing, right? I think it'll come down to investors to be showing our dataset when we do show it, and assuming it holds up, and asking rheumatologists, "Do you think that rituximab alone or Cy/Flu could have done this?" And even if some people push back in the beginning and say, "Well, I'd like to see more follow-up to really make sure that that's the case," over time, this becomes pretty clear, right? So our expectation is that our regimen would never have driven the complete responses and the durability that we've seen in cancer. Our expectation today is that the individual components will never be able to drive the types of efficacy that we're hoping we can achieve. As you mentioned previously, Artiva is prioritizing RA among a basket of other indications in autoimmunity. What is the bar now looking forward to this readout for AlloNK in the upcoming readout as it relates to ACR50 or safety? What should we be looking for? Yeah. RA, as you know, Gil, is the largest autoimmune indication. And there are many approved drugs in RA. So I have heard this from other people. Well, is there really an unmet need in RA? And the reality is that all of the clinical trials, I think I can say this, all of the registrational trials that have been run in RA have been focused on patients that had never been on a biologic or a targeted synthetic or had maybe failed one. Nobody has actually run a registrational trial in patients that have actually failed two distinct targeted mechanisms. So let's talk about the ACR50. The ACR50 is, in a way, the gold standard for regulatory purposes of determining whether you are driving a response or not, and it's usually measured at six months. As I mentioned, I like the fact that it's six months because we have seen in the literature that sometimes the steroid pre-medications that one gives with all the modalities that we use in B-cell depletion or the Cy/Flu may still have lingering effects at three months. By the time you get to six months, those effects are largely gone, and now you can have a real appreciation for whether the drug is working or not. So the ACR50, w hen you look at the ACR50, the percentage of patients that achieve an ACR50 response when they're taking their first biologic or a JAK, it's in the 35%-45%. Now you look at what the ACR50 is. If you've now failed either, let's say, a TNF or a JAK, and now you're going into another class that you haven't been on, that now drops to 20%-35%. And then when you look at what the ACR50 looks like for patients that have actually failed two distinct mechanisms, it drops into the 10%-20% range. Right? Said differently, you fail two different distinct mechanisms, and now you're going into a third. There are many to choose from. You're going into your third, and you only have a 10%-20% chance of actually having an ACR50 response to what's available. We are proposing that we have the possibility, the potential, we are driving towards having 50% of the patients achieve an ACR50, which really would be one of the highest ACR50 responses that we have seen in the context of RA, and we're doing it in a late-line setting, as opposed to many of the other drugs that go into RA that are focused on the earlier-line setting. So we believe there's a very big unmet need here. 25% of the patients that ever start taking a biologic or a JAK, eventually have an inadequate response to two distinct mechanisms. It's actually a large percentage of the population today that are on all these branded drugs that don't get much relief from the drug they're on. So we believe that because of the deep B-cell mechanism, which promises to be quite impactful in autoimmune disease because we believe that we can drive efficacy that one has not seen with other mechanisms, and because of the safety profile that we talked about in the last question, we believe that we could actually make quite a big difference in RA. And very importantly, we strategically did our activities so we could be first, right? Because whoever is first with a compelling target product profile across these indications is going to be fairly attractive as a company and as a product. And so as far as we can tell, we are the first company to talk to FDA about a registrational trial in RA. And if those conversations go well, then we could be the first one to start a pivotal trial in RA, and potentially the first to market with an agent that has the potential to drive a lot of relief in these unmet need patients. Clinical study status question. You mentioned we're going to be looking at about 15 patients. How many patients do you have enrolled, and what kind of length of follow-up are we talking here? Yeah. So we, in our last update, which was in the October-November timeframe, we stated that we had treated 32 autoimmunity patients as of an October first cutoff. I think that's pretty impressive, right? I think we have enrolled as well as anybody else, which speaks to the ease of use of our product and how attractive it has been to PIs. Since then, we have continued to enroll quite nicely. I will provide a more detailed update on that when we do provide the full data update that we're planning to provide. Specifically what we guided for is that we would have at least 15 RA patients, and this is important. We've seen small data sets from different companies, and I think you need a large enough data set to start drawing conclusions. With the majority of those 15 patients having six or more months of follow-up, which are important for the reasons I mentioned, which is sometimes at 12 weeks, you can still see the residual effects of the pretreatment. By six months, you start to have a feel for whether this is looking durable or not. We treated our very first RA patient, because we announced that, around 12-18 months ago. We will have at least one or two patients that will have longer follow-up than the six months that I'm mentioning. But f or now, we are trying to show directionality in the degree of response. We are trying to show that this isn't not durable, and I say not durable because there's been papers written about data sets at three months that later on turned out to actually not have a durable response by six months. At least six months tells you that this is something that has the potential to be durable, but we have to be realistic, that we're going to have to wait until EULAR in 2027 to actually see data sets that have 12, 24 months of follow-up for us to have a true appreciation of how durable this therapy can be in RA. You're right on to the next point here. What kind of durability makes a product? I know we're talking about six months, and that's the time point we're going to be looking at, but in your view, you're a drug developer, what kind of durability do you think makes a product in this space? Look, in my mind, the longer that durability is, of course, the more compelling it is, right? Because during that period, when a patient is in response, they're not on any other immunomodulatory drug, which means that they have the possibility of having a lower risk of infection than they currently do today on JAKs, or TNFs, or all the other drugs that are out there. We feel that 18 months, a median duration of response of at least 18 months would be very compelling. Because again, we're not talking about first-line patients. We're talking about patients that have already failed two targeted mechanisms, and now they're going to a third. And the guidelines state very clearly, if you're on a third mechanism now, at six months, if you have not benefited from the drug, you're supposed to change to a fourth, and then you go to a fifth. We are talking about having a therapy, if it does have a median duration of response of at least 18 months, in patients that may have just been cycled through two or three different drugs. In the meantime, our patients, if they do receive that benefit, they could have been off any immunomodulatory drugs. We believe that that would be a very compelling bogey, given the fact that we are using Cy/Flu, so this isn't going to be for everyone, and given the fact that we are dealing with patients that are actually quite refractory. How do you view redosing, especially given the Cy/Flu angle? Yeah. There are two opportunities to redose scientifically, right? One opportunity to redose, which we are starting to explore in our current basket study, is the idea that if you treat somebody and they're not showing a great response, what happens if you treat them again at six months? Could you then, with that second treatment, drive them into a reset? It's an oncology strategy. Yeah. Yes. This absolutely cannot be a therapy that you're giving every six months because it does utilize Cy/Flu. So one redosing strategy would be to get somebody into a reset with a durable response. The second strategy is if you do get someone into a response, what do you do if they eventually, down the road, lose that response? If you re-treat them, then can you actually drive them back to a response, and will that response be as durable as it was in the first go-around? What I can tell you, we can start to generate data around this first opportunity of what do you do in patients that are not responding. Hopefully, there aren't that many patients not responding. More importantly is what happens at retreatment 12, 18, 24 months later. That's going to take a long time for us to be able to generate that data, because we need to have patients that have enough follow-up to lose their response for us to then re-treat, and then for us to see whether we can get another long, durable response out of them. Those are the two retreatment strategies, scientifically, that one would think about. I personally think that the most important one for us to establish is really that re-treating somebody after they had a reset, but then they have a loss of response down the road. Because that would open up the possibility that, imagine, Gil, you could keep one of these patients for a decade under control by having them come in every 18, 24, 36 months, and getting a few infusions, and being done with it. Well, that's absolutely fair. I do want to spend another second here on the safety profile. Just again, to emphasize for everyone that this is not a CAR T, it doesn't have the CRS and ICANS that's associated with that kind of product. Yes, that's correct. If we start with the cell therapy side effects, we have no CRS. We've had no ICANS. I'm referring back to the 32 patients that we presented in November. We'll provide a more fuller safety update when we do our data reveal. We saw no CRS, we saw no ICANS, we saw no need for tocilizumab to drive runaway CRS. We saw no IVIG necessary because of hypogammaglobulinemia. As far as the classical side effects that we're seeing with the T-cell approaches, whether it's auto CAR T, whether it's TCEs, we don't see any of that. Really, the side effects of our therapy, again, looking back to the data that we presented in November, they were the known side effects of cyclophosphamide that physicians know well, fludarabine, there's been extensive experience with it, not necessarily in rheumatology, but definitely in oncology, and the side effects of rituximab. With the Cy/Flu, what are you really looking for? We know that the Cy/Flu causes cytopenias in these patients, but these cytopenias are very transient. They last two to three weeks for the most part. While these cytopenias are happening, physicians are giving these patients prophylactic anti-infectives. They're protected during those two to three weeks. For us, the data set that we presented in November was actually quite important because that was a data set on 32 patients. A look at the first 28 days when they were cytopenic to ask the question, do you end up getting a lot of hospitalizations because these patients are cytopenic? The answer was no, you don't. If you're not getting a lot of infections with these patients, then what are the other consequences of Cy/Flu? Well, patients can get nauseated from taking it upfront. We only give it for three days, and it's a low dose. The remaining long-term theoretical concerns are a little bit misunderstood by investors. Number one, people talk about concerns around secondary malignancy. Those are very well established in the literature that they only happen at very high doses. There is no evidence in the literature that at the doses that we're using, that one has concerns around secondary malignancy. You have the question about fertility. Fertility, again, is less understood, but fertility is a hotter issue. That's a very personal issue, and many physicians are going to feel a little hesitant to offer lymphodepletion to young female patients of reproductive age that still want to build a family. One of the reasons we like RA is that the vast majority of patients in RA are not in that situation. When you put it all together, the lymphodepletion is a cytopenia that you're following with a lab value. Unless it manifests itself in a symptom that you have to address or treat or to hospitalize a patient for, it can actually be quite tolerable. There was no opportunity for the world to know how tolerable Cy/Flu can be until we came along with a therapy that with rituximab and our NK cells, there really aren't any major unexpected side effects that you expect from those. You can finally see what Cy/Flu does at these low doses on its own in our patients, because there won't be other more serious side effects like with auto CAR T masking the tolerability of Cy/Flu. How do you think rheumatologists are going to receive the use of LD? What kind of education efforts are you looking ahead of you as some things work out? Yeah, look, I can tell you, we think a lot about this journey. Because I find that rheumatologists are being bombarded with questions about lymphodepletion in a vacuum. They're being called, and they're asking, "Hey, how do you feel about Cy/Flu?" That's how they're being asked the question. They're not being asked the question, "Listen, I'm going to tell you about a drug that can actually drive your patients that don't respond to the approved drugs to actually have a much higher response rate, and for them to potentially have a durable response that could last 18 months or more." After you explain that, then ask the question, "Well, what about if you have to give Cy/Flu at the beginning, and these are the consequences of Cy/Flu?" You're not seeing higher hospitalizations, you're not seeing higher infection rates. How do you feel about the overall target product profile? I think that the way they'll come along is once they see why they're using the Cy/Flu. If you just ask them about Cy/Flu, who wants to give Cy/Flu? If you actually offer a therapy that can provide a lot of relief to their patients, and then you ask the question about Cy/Flu, now you're going to get a holistic answer. The other thing I can tell you is our experience in our clinical trial. 95%+ of the patients that we have treated have been treated in a community rheumatology practice where the rheumatologist is administering the Cy/Flu and the rituximab and the cells, and they're monitoring our patients. Every single one in the beginning is like, gee, I've never used fludarabine before, what is that like? You walk them through it, you explain it. For the very first one, they're a little bit on edge, just making sure that there isn't going to be a problem. Once they start using, the feedback that we get is, "This is actually quite easy to use." That is before we have an opportunity to have a large enough efficacy data set with enough durability to then really show them what we're doing it for. I do want to spend also a second on the data that was presented from the 32 patients. It's a little bit of a conundrum in my view. You didn't get a ton of recognition for this data set. These patients have really long B-cell aplasias. Assuming you understand the mechanism of how resets work, is there any reason why such a long B-cell aplasia in serum won't translate into immune reset? Just looking at other data sets, I don't think others have put out biopsy data sets. That's probably more accurate. At the same time, just looking at serum data sets, why would investors think that this doesn't work? Well, look, I think a couple of things. You and I have spoken about the importance of a high sensitivity assay, right? Yeah. If you're not using a high sensitivity B-cell assay and you're presenting B-cell depletion the way everybody does, even rituximab can actually show you a B-cell aplasia that lasts six months. As we know, the problem with rituximab is that it's an incomplete depleter. If you actually measure B-cell levels using a high sensitivity assay with rituximab only, one can see that the average patient still has B cells that will not be detected by the standard assays, but they will be detected by the high sensitivity assays. To your point, what I think we showed that was not as appreciated as it should, is that in every patient that we treated using our regimen, using a high sensitivity assay, we saw no detectable B cells. Using a very similar assay as all the studies out there that show that the average patient on rituximab does have still B cells present even after they take rituximab. I agree with you. The mechanism of action that we're pursuing, that Chad explained, is that you need to have a very deep B-cell depletion quickly. Maybe only hitting it really hard enough up front. We know auto CAR T hits it hard, and it hits it quickly, and then it goes away because you start to see B cells coming back at 90 days-120 days. Our hypothesis is exactly the same. If we can drive B cells depleted very deeply, and we're not seeing any in the periphery, which is a great first step, then why shouldn't that translate into good efficacy? Obviously the proof is going to be in the pudding once we actually come out with efficacy data, and then more importantly, down the road, with durable efficacy data, because then we'll have explained the entire thing. There's another important aspect of the technology, and that's the manufacturing. Just to put this in perspective for people who follow the cell therapy space, what kind of scalability and consistency we're talking about here and the kind of capital requirements that you guys would need in order to move forward? This is a really important point, and I think it'll start getting more appreciated once people move on from mechanism of action, and they move on to business model, right? We have a highly scalable process. When Artiva was founded in 2019, this is a process that had been worked on for 10 years by our partner, GC Cell. We are actually a spinoff of GC Cell. We have the ex-Asian rights to this technology. From one umbilical cord unit, that's where we source our NK cells from. From one umbilical cord unit, we can make four trillion cells. Trillions, what does that really mean? It's hard for people to understand what that means. Putting it in terms of number of patients, one umbilical cord unit would allow us to treat between 500-1,000 patients, right? I bring up this notion of trillions because the one big advantage of NK cells, people don't boil it down to this, but to me, the one advantage of NK cells is you don't have the therapeutic index that T-cell approaches have. You can hit it hard and have a very deep depletion without the side effect issues. The disadvantage of NK cells is that you have to give two orders of magnitude more NK cells than the CAR T companies have to do. That poses a challenge, unless you have something that is highly scalable. Why are we so scalable? Number one, because we're not genetically engineering the cells. That makes a big difference. Whenever you introduce genetic variation into the cells, you have a yield hit. There can be differences on how the cells take the genetic engineering. We are not genetically engineered, and because this process has been worked on for so long, this operates a lot like a biologic. You have your starting material, you expand it into intermediates, you put it in a bioreactor, it grows, and then you collect it from the bioreactor. When you think about it, that's how you make monoclonal antibodies also. You are also growing them in cells that you're growing in a bioreactor, and then you're extracting them. We have downstairs a 9,000 sq ft facility that at capacity, 9,000, just think about how big that is. At capacity, that could treat 500-1,000 patients, just that. When we actually start being more forthcoming with the investments that will be required to scale this to become a billion-dollar product, you will see that this isn't an order of magnitude more than a biologic the way auto CAR T is. This is a lot closer to a biologic than one would expect because our process is so mature and we're not engineering it. Speaking of positioning, and because you mentioned the biologics, we sometimes hear that biologics and bispecifics are already pretty effective and they're relatively easy to use. How do you think about the opportunity for single use or finite duration therapy in autoimmune disease, which is kind of the premise of a cell therapy? I think that one of the limitations that all of us in cell therapy, particularly all of us that use Cy/Flu, is that this better be a one and done. Right With durability because this can't do immune dimming like the biologics can do, right? I would argue that we started with rituximab, which is an inadequate B-cell depleter. Obviously, it's been efficacious. We've been using it. Hundreds of thousands of patients have been on it. What Thad showed us was the possibility of a reset, right? With the reset, you get that durable response. I think what we're learning from the TCEs is that we have not quite seen very durable TCE data sets. I followed these data sets very closely. Erlogen, I would argue, are the ones with the most experience with TCEs. We are not seeing the degree of durability that Erlogen is seeing with auto CAR T. They recently introduced the concept of immune dimming, not immune reset, but immune dimming. More of a chronic therapy that you can give, which I would call rituximab plus. Right? Because that rituximab is a dimmer, but maybe you would argue you could have better dimmers. Look, I think that there's room for a lot of people, but I do think that a dimming strategy is more complicated because you have to choose a dose, you have to choose how often you're going to be giving it in order to determine what that's going to be like. You have to navigate your therapeutic index. I have no doubts we're going to see TCEs succeed in the clinic. What we're trying to do is to be first in the market with a therapy that can pursue the one and done. I don't worry about the TCEs in the sense that there's room for a lot of people, and they will have their own place. If you are a community rheumatologist, if you today give IV drugs for RA, our product would fit right into your reimbursement pattern, to your clinical operations activity. We feel that particularly when we go after big indications like RA, that there is really room for a lot of people, and the target product profile is going to determine how much of each product people are going to use. Maybe another point worth mentioning as it relates to T cell engagers, and they still have some of the CRS and ICANS toxicities, even though at a very low rate. I don't know what kind of feedback you've gotten from physicians, but I've heard very low tolerance for this in the community. Yeah. Look, what I am hearing is that there is definitely a therapeutic index that TCEs have to think about. Let's be clear. I don't think anybody pretends like there isn't one, which is if you want to develop a very high efficacy TCE, particularly with a 1st-generation TCE, not these 2nd-generations that have been detuned their CD3, you are going to have to choose whether you go for very high efficacy. That will come with CRS, hypogammaglobulinemia, revaccination, or you're going to go for a dimming strategy where you're using a lower dose, which won't be as efficacious. It means you're going to have to dose it chronically, but you'll probably get a safety profile that is a lot more accessible. I think those are going to be the options, at least for the first-generation TCEs, if not for some of the ones that are already further along in the second-generation. Over time, people can think of more selective ways to try to do it. I think for now, those are going to be the choices for the TCEs. We have an opportunity to move ahead of that and move quickly by actually following the one-and-done, because that is what we have to do. Either we succeed with the one-and-done strategy, which we are confident about, or we don't succeed because dimming is not an option for us. We're going for reset. Just to remind our audience, last few minutes here, cash position, runway, kind of how are you viewing the market? Yeah. We ended 2025 with $108 million in cash, and we guided that we have sufficient runway to get us into Q2 of 2027. If you have any last comments, something you'd really want to highlight for investors or something you think we hadn't touched upon that you feel is important? Yeah. The one thing I would highlight to investors is every conversation that I go to an investor is immediately, "Oh, let's talk about all the different modalities that are depleting B cells, and let's have a conversation about how one compares with the other." I want people to move away from that and to say, "Okay, you're going into RA. Is there an unmet need in RA? When are you going to get to that market? What could you sell this for? Is anybody else going to beat you? Do you have the opportunity for a good target product profile? How would rheumatologists embrace this in the context of RA? The standard questions that we ask biotech companies that have promising products in interesting unmet needs, and I'd like to move away from the can we talk mechanistically because this one says dual targeting versus single targeting, and this B-cell subpopulation and the recurrence of naive B-cells. That's all really interesting, but at the end of the day, we need to develop a drug that works, that's safe enough, and that addresses unmet needs. That's the transition that I'm hoping to get to soon. To translate, let's move away from talking about platforms and start talking about actual drugs in patients. Exactly, because that's what matters. Okay. Fred, we're pretty much at time. I want to thank you again for attending today. Thank you, Gil. Really appreciate your support.