So let's get started. You're recently public. You got a very, very interesting platform in I&I, so let's talk about Zenas. Maybe just give a very quick high-level overview of the platform, how you started the company, the key asset, and then we'll dig in. That sounds great, Yigal. We appreciate being here. Let me just refer anyone in attendance or online to our SEC filings. We'll be making some statements here that those apply to. But from an overview standpoint, I think this is clear. We're an immunology-based company focused on autoimmune disease. We've built this company to immediately jump into multiple clinical trials. So we have global capabilities, meaning we have clinical operations teams on the ground in Asia, Europe, and North America. It's a very experienced team of people that have been associated with multiple drug approvals in the past. And they're focused on our franchise molecule, Obexelimab, that we'll, of course, talk quite a bit about recently having completed enrollment in its very first phase three trial for IgG4-related disease. And the company, following the crossover round and IPO this year, is well capitalized through a number of milestones, of course. We built the company's pipeline through business development. We intend to continue to do that. Just a quick summary for this year, which has been a tremendous year for the company. If you think about the fact that we did two substantial raises, the crossover round, bringing in $200 million, the IPO, over $250 million, completed the enrollment of the IgG4-RD study, and importantly, started two additional studies for obexelimab, both of those being global randomized phase two trials, one in multiple sclerosis we'll discuss, I'm sure, and one in lupus. And we recently, as of yesterday, released some interim results on the pilot proof of mechanism wAIHA study. We can jump into that and build out the management team. But it's all about execution. This is a team that has completed three trials. There's five ongoing. Globally, 220 clinical sites in 31 countries, well over 300 patients enrolled. So we'll just continue executing and delivering what we think are potentially value-driving milestones. And you can see here for the IgG4-RD phase three study, the INDIGO study, with the study completing enrollment mid-November, that means last patient out will be mid-November in 2025 with a 52-week endpoint. And then, obviously, all those things that need to be done to lock a database and analyze. So about year-end next year, we'll have the top-line phase three results. But before that, the MS trial will be reporting out in the third quarter of next year. And we can talk a bit more about that. And the lupus trial will finish enrolling next year. So I think that sets us up really well. Okay. You touched on all the key points. So we're going to go into each of those in a lot more detail. But just at a high level, let's just talk about the therapeutic hypothesis, B-cell inhibition versus B-cell depletion. That's obviously a central theme in everything you are doing. You had some data. You mentioned that you released yesterday some new slides. We'd love to have you walk us through that. And then the POC, the proof of concept in this way, which we understand you're not going to take forward for yourself, but still it provides some very nice read-through in terms of the MOA for obexelimab. So why don't we hit on that, and then we can come back to IgG4 and the other stuff. Okay. So as a foundation, just as a reminder, when we brought obexelimab to the company, we had a wealth of data to first conduct diligence on. And what we found from the non-clinical data was tremendous support for the mechanistic aspects of the drug as a potent, rapid, and sustainable inhibitor of B-cell lineage. But that was supported by clinical data, which is listed here just quickly. There was a multiple-ascending dose trial in rheumatoid arthritis with this drug. And if you look at on the slide here, the ACR 20, 50, and ACR 70, this is an active drug in rheumatoid arthritis. At the time, Xencor had it in their hands. And with TNF alphas dominating the market, it wasn't a thing for a young biotech company to jump into rheumatoid arthritis, but clearly active. Then a phase two pilot study in IgG4-RD, as you mentioned. We'll dive into that further, but having data in hand that showed a 93% sustained response, an induction study where these patients were put into response and then sustained in response. Then a lupus study that, although this used an older formulation that didn't provide the right exposure and target coverage, there was still activity. The intent to treat population did 17% better than placebo. That's what the marketed drugs did. But in a population where exposure was where it needs to be, and it will get there with our subcutaneous regimen we're using now, the effect size was 35%. So we had non-clinical data, but also the clinical data supporting this mechanism. Specifically, I'm not going to spend time on why CD19 is a great target because I think everyone understands why CD19 is so relevant, hitting most of the lineage of B cells, even a subpopulation of plasma cells. Importantly, if we look mechanistically at Obexelimab, as you know, it co-engages CD19. Really, it's the Fc gamma RIIb or CD32B binding that drives the inhibitory signal rapidly and potently in B-cell lineage, as depicted on this slide. The molecule is devoid of ADCC, so it doesn't deplete. We think if you look at the non-clinical data, and if we have time and you want to go into that, there are a number of experiments we can touch on that support the fact that it decreases antibody production, it impacts cytokine production, antigen processing and presentation to T cells, and progression in lineage to become plasmablasts and plasma cells, all via this mechanism. So we landed on a dosing regimen, and I'll show you some specifics here about the dosing regimen that provides target coverage in a sustainable fashion. This is a subcutaneous weekly administration. And in maintaining high C-trough, and you can see on this slide with a mean C-trough of 17 compared to the older regimen of three, it's greater than a five-times increase in C-trough, we have continuous pressure on B cells and tissue. So that's really important autoimmune disease. We know that depleting antibodies may be somewhat of a misnomer. I think true depletion comes from CAR-Ts. From anti-CD20s, anti-CD19, you get profound depletion in the blood compartment, but not complete depletion in tissue. So with our continuous dosing versus the dosing of those agents, which is typically every six months, and there's variability with every six months as to how deep the tissue depletion is, and then how soon patients replete, we think we can provide greater coverage. And over time, not have that window when patients are exposed and not have complete efficacy. So we think the dosing regimen we picked here provides that differentiation. And then additionally, I think it's recognized that if you pause our drug, since it's not a depleter, B-cell activity returns. So patients can potentially be vaccinated or manage clinical sequelae, for instance, from an infection. Just to jump in there, how quickly does it return? Because that's an important point relative to the B-cell suppression curve with. Yeah, in a matter of weeks. Okay. Yeah. You want to touch quickly on the wAIHA? Yeah, yeah. Let's jump to that. I'm going to advance some slides here. Bear with me as we go right to that because I think this is a really important data point that once again demonstrates mechanistically what this drug can do and clinically what it can do. This is a, I would have referred to this as a pilot study of proof of mechanism. It's a single-arm study in patients with wAIHA, where we looked at hemoglobin measures and other clinical measures, red blood cells, LDH, bilirubin. What you see here in the chart is over the 24-week period, the actual change in hemoglobin. This is for the eight patients who were eligible for analysis. We've actually enrolled nine, but one only had four weeks of data at this point. You can see the increase of hemoglobin. Importantly, five of the eight patients actually had from a nadir to the peak hemoglobin a two-gram per deciliter change. There was about a 25% increase in red blood cell count, a 25% decrease in LDH, so what this is demonstrating, obviously, is impacting first the destruction of red blood cells, and then secondly, allowing for the replenishment of red blood cells sustained over time, and as is the case with all of the studies, the drug was well tolerated, and I highlight one thing on here. There's primary wAIHA, and there's wAIHA secondary to autoimmune disease. There was one patient that had wAIHA secondary to autoimmune disease. It was autoimmune hepatitis, and that's the chart here, and you can see this patient with a rapid increase in hemoglobin, ultimately over a three-gram per deciliter increase and significant decline in LDH and bilirubin. I think it's a really nice case study, especially with this being autoimmune-based. Yeah, very nice. Okay. So let's switch back over then to the lead indication to IgG4-related disease. So first off, it's not an indication that everyone is super familiar with. It's recently been sort of explained by some of the experts. So maybe just give us an overview. What exactly is it? How does it manifest? What's the market size? You quickly mentioned the phase two data, but let's drill into that a little bit more. And then we're going to walk through your phase three. Okay. So I guess you would call it a newer disease. It was first identified in, I think, 2003. It's called IgG4-RD or IgG4-related disease. Recognize that the IgG4 isn't because of IgG4 blood levels being increased, although those frequently are. It was named IgG4-RD because upon biopsy, there's a high level of IgG4 staining that occurs with localized plasmablasts and plasma cells. That's where the name came from. But it's a disease that affects multiple organs leading to fibrosis. Patients present typically in flare, and with that flare, they have to be treated, or it will lead to that fibrotic lesion in the organ, decreasing organ function over time, so it's important to control flares, no approved drugs. Corticosteroids are effective, but patients can't sustain on them. There are probably over 20,000 patients diagnosed in the U.S. with the disease. Some people believe it's much greater than that, but let's stick with that now because that we have solid data on. Like many autoimmune diseases, initially, the population is estimated at one size, but once there are drugs that are available to actually treat the patients, more patients are typically diagnosed. In addition, an ICD-10 code was put in place just about a year ago, so that over time will accumulate more data. Same thing in Europe, over 20,000 patients probably diagnosed today, and the disease, it's obvious that if you impact B cells, you can make a difference here, so let's move on a little bit here. I want to share something with you from a data standpoint. When we brought this drug in, we already had phase 2 data, and this was conducted at Mass General by one of the leaders in the field. You'll see one column that's labeled Obexelimab. The other column is labeled Rituximab because that same center led a similar pilot trial. And what I would suggest here, it's a nice way to think about our inhibitory approach compared to a quote-unquote depleting approach with an agent that's effective. Although there are no randomized trials in Rituximab and it doesn't have a label, it's utilized today because there are no other choices except for steroids. Obviously, with ultimately an approval of Uplizna from Amgen and then Obexelimab, there'll be choices for physicians. But the baseline characteristics were quite similar, as you can see, the number of organs involved, the RI score for both. And the primary endpoint, numerically better for Obexelimab, but similar. Importantly, glucocorticoid use, no patients after tapering needed glucocorticoids in our study. In the Rituximab study, 10% received them. And then sustained disease response. This is all the way to the end of the study, 93% in the Obexelimab study, 73% in the Rituximab study. And I would point to that being the concept I brought up earlier that with this every six-month regimen, as you get to the end of the six months, some patients or the benefit of a depleting antibody may wane. And that's what I believe we're seeing here. The other important point to point out or to emphasize is how quickly the drug works. So for Obexelimab, the time to disease response was 21 days. It was 43 days for the depleting antibody Rituximab. So clearly, it's a rapid onset and relapses are rare. Just on this study, just to be clear, these are not two arms within the same study. These are two separate studies. Two separate studies, but of similar scale, same center. The same. There's a reason for comparability. That's right. Okay. It's always unfair to do cross-comparisons, but we all do it if it's the only information we have. But for well-understood antibodies, I think it's a reasonable thing to do. Okay. In the hands of the same investigator. Yeah, yeah. Okay. Very good. This is another way to depict our data. You see the rapid decrease in the IgG4-RD responder index or RI on the Y-axis when the drug is administered. This is the induction phase, right? Then the maintenance phase that is sustained. That leads to the phase 3, which is a maintenance study. Steroids are used for induction there. But we know the drug is extremely active because it works so well even in an induction phase. If you understand that point. Yep, yep, yep. Okay. All right. So let's talk about, you mentioned Uplizna a few times. So maybe we'll do that part first. So let's talk about how you see, obviously, Amgen showing their phase 3 data. They had a presentation recently. So let's just talk about the competitive profiles for both agents, how you see yours differentiated. Clearly, the depletion versus inhibition is an important feature. There are others, though, in terms of route of administration. So let's kind of talk about that and how you see the market shaping up. And of course, Rituximab, as you mentioned, off-label, used in some fancy centers, but maybe tough to prescribe in sort of an ordinary community center. Yeah. So obviously, steroids work, but are problematic long-term. We know that. Rituximab is beneficial. No randomized data, not a label. Rituximab is used and actually paid for in other diseases where it has randomized data, but is off-label. But here, there's no randomized label data. And it can be obtained. It takes typically multiple reviews by a payer. Some of the larger centers have an easier time of that. But for many clinicians and patients, it's very hard to access because it doesn't have the appropriate clinical evidence. As we go forward and we look at Uplizna and obexelimab, obviously, there's a role for both. The data set from Uplizna from the phase 3 study showed that the phase 3 design is an appropriate design, that the placebo arm in that study had a flare rate of 60%, which says maintenance therapy is really important. How do the two differentiate? As you mentioned, Uplizna is an IV infusion that involves going to a center, first getting access to a center, getting scheduled, going, getting pre-medication, then the infusion of the drug, and then the monitoring. And that's important because even in the phase 3 study of that drug, with pre-medication, there was a 19% infusion hypersensitivity reaction level, which isn't surprising. Rituximab has about a 20% hypersensitivity reaction level with infusion. So I think that's an important differentiation. Ultimately, with Obexelimab, with our development program for an autoinjector, the patients would typically get their 30- or 60- or 90-day box of autoinjectors, just like they do for many autoimmune diseases, for obesity. I mean, autoinjectors are like a standard now. And they do their less than 10-second autoinjection once a week. And I think for many patients, that's a much more convenient approach. I think there's been enough studies looking at what patients prefer an at-home autoinjection or going to an infusion center. And most all the data suggests they prefer to have that control of their own disease and to do it at home. I'd point out, actually, in our initiation report that we wrote on Zenas, we have some very good data on that point. So I think both drugs will have a role. Obviously, the repletion associated with an antibody, an Anti-CD20 or an Anti-CD19 antibody takes time. It could take four or five months, but for some patients, it could take nine months. So if there's clinical sequelae, it's problematic vaccinating those patients. So I think there can be some differentiation there too that I would underline. Okay. And then you mentioned the timelines. So, November, final patient, last visit, or around that time next year, and then the top-line data. Let's talk a little bit before we go to lupus and MS. Let's just talk a little about the commercialization. What have you done in terms of the prep for the commercialization for Obexelimab at this point? So we have, as I listed on the first slide, we hired our chief commercial officer, and we have a market access person. We have our data analytics person. Obviously, having a team that's brought multiple products to the market in North America and Europe in the past, we sort of have a roadmap on how to do that. This is a narrowly targeted audience. This is rheumatology primarily with a little bit of gastroenterology, those gastroenterologists who may see liver and pancreatic disease, which shows up as IgG4-RD. So it's a targeted audience. And at this point in time, we have a very active medical affairs group with medical science liaisons in the field, scientific communications group doing the work that they do. So we're laying the groundwork for a successful launch, and we have the team that can do that. Okay. You started talking about lupus a little bit, but let's kind of go into a little more detail. So the Xencor study, let's just understand exactly what happened there. It sounds like there was some analysis considerations that may not have been ideal in terms of how that was done. So can you walk us through that and why you could see beyond that in terms of pulling the trigger to do the deal? Sure. And this goes back to some degree what I said about the proper exposure to have target engagement, to not let that decline based on C-trough. So first thing I would say is the lupus study that had been conducted, the phase two A study depicted here, utilized the IV regimen. And we know that all of the benefit in the study was seen in patients that had a C-trough above the median. So it's really important to keep C-trough up. Overall, the study used an efficacy-evaluable primary endpoint analysis. And unfortunately, there was a high level of placebo dropouts in the study. Those were removed from the denominator in the EE analysis, which enhanced the placebo benefit rate. It brought it all the way to 29%. Now, the study was designed with placebo only having a 10%. It ended up being 29%. So there were only 50 patients per arm. But when looking at the ITT population, which is the more classical way, typically the conservative way to do it, the actual effect size I had mentioned earlier was 17% as described on this slide on the primary endpoint. And importantly, the optimized exposure delivered 35%. And then the other thing done in this study was exploratory biomarker analysis, retrospective, a small N, but quite intriguing where the effect size jumped all the way up over 50%. So when we look at this before we in-licensed the drug, it was clear to us you had to get exposure to the right level. And the subcutaneous regimen does that. Everybody has a C-trough, if you saw before. That's five times, well, the mean is five times higher than the C-trough of how this drug was administered in this study. But everyone in our study going forward in lupus will have a C-trough above that median. So that was important. In addition, when you think about lupus studies, you need to do everything you can to tighten up the patients who are enrolled, the eligibility criteria. Sometimes that's skirted a bit by investigators. So what we're using in the study listed here, and this is our randomized phase two that's ongoing with 95 patients per arm, it's doubled the size approximately of the prior study. And adjudication committee to the far left on this graphic has to confirm the screening before the patient gets into the study. That's critical. And then we use the newer EULAR guidelines of five milligrams of Prednisone equivalent to keep the control arm response down. So the proper regimen, upfront criteria adhered to, lowering the steroid, and obviously sizing the trial properly. That's why we have confidence. This drug is active in this area, and we think we've optimized this chance for success. In addition, because there are other lupus studies, we know that, right? There are a lot. This is the one study that includes leading-edge biomarker analysis. So a lot of the rheumatologists are excited about this. So in conducting lupus studies, I know there are a lot of studies out there, but any one center will only have one to three studies. So once you're in the center, it's just ensuring you're getting your fair share of patients. And the kind of patients we're getting are frequently different than, for instance, the CAR-T lupus study patients. And that's a whole complicated oncology rheumatology collaboration at the site anyway. So getting into the sites, it's first is the most important thing. And the way we get into the sites is because we're doing biomarker work and the trial's enrolling. Now, have you talked much about what biomarkers? I don't think that you can go a little bit more. We can because some of this was published from the Xencor trial. So these patients have RNA sequencing being done. When we've all learned from oncology how straightforward that really is. And there are gene profiles, patterns, endotypes. It depends on who's doing the analysis. And we're using two major groups, actually three groups to do the analysis, one academic and two are commercial entities applying their algorithms. And we actually put the prior data in the other study into their hands, and they did the analysis. And it's 30-plus% of the patients that meet those. And we're looking to confirm that here. And then we have a few blood markers that we haven't discussed as much that we're looking at. And we'll see what comes out of that to then utilize potentially in the phase three program. And the other sort of conceptual question in terms of order of operations, when you saw this Xencor data and you looked at it closely, at that point, did you in-license based on conviction there? And then IgG4 came later, or was that already part of the broader plan when you were looking at SLE? That's a great question. We actually, over time, looked at about 40 indications, and we narrowed it down to a half dozen, and some of those we're prosecuting right now. Our initial look was at Lupus. Lupus was the foundation for in-licensing the drug, always planning to do IgG4-RD also because IgG4-RD, if you think about it as a young, at the time, private company funding a single-arm trial of about 200 patients to get approval, that's a very capital-efficient indication, a growing indication. That was kind of a given, but most of the work was about Lupus. The data, as we dug into it, got us very excited. Okay. And as far as the market size and that 30% that meet those biomarker thresholds, what are we talking about in terms of a TAM? Yeah. So I think. I'm sure you have a slide on that. Yeah. If you look at the overall lupus population here and you think about the pricing that's garnered here, put it against the population, and if it was just a third of the potential 9 billion that's estimated, which is the biomarker population, it's still significant. I wouldn't necessarily focus just on the biomarker population. I think it's really interesting to be doing that work, but where that takes us in phase three, we don't know yet But I would refer to the oncology paradigm where if you have an active drug in the overall population, you still may set up a phase three looking at a biomarker population in your primary analysis first statistically in your hierarchy, take an alpha hit, and then test your overall population. So think about PD-1 inhibitors, think about PARP inhibitors, think about some of the other precision oncology drugs where that type of trial design has been quite effective. That's something we could think about here. But let's see what comes out with the phase two. And then when would you consider starting a phase? Presumably, the phase two looks good. How quickly could you start a phase three in lupus? Or you would wait till the IgG4 reads out? If you think about it, the lupus study, and we've accommodated this in our timelines because it's going to take longer than the MS and, of course, the IgG4-RD study. We will finish enrollment next year, and it'll report out in the first half of 2026. Based on that, we'll be doing phase three planning. Clearly, any phase three advancement would be after the IgG4-RD readout and after the multiple sclerosis readout. Okay. Let's make sure we get to multiple sclerosis, which is kind of going in inverse order, the biggest opportunity by, I would say, an order of magnitude, at least relative to lupus. Here you have some very interesting preclinical data, no clinical data with obexelimab that I'm aware of yet. So tell us about, maybe we can go to the slide with that very nice, yeah, let's talk through that first. Yeah. I think whatever value anyone would put in an EAE model, it is the model. Yeah. Right. And what you see here is the model comparing the Obexelimab surrogate, which is necessary in this mouse model versus an anti-CD20 antibody. And we know that anti-CD20 antibodies are quite effective clinically, in fact, approaching $9 billion in sales with 50%-60% of all MS therapy being anti-CD20 antibodies. So what we see in this model, of course, is the administration of MOG and then tracking on a clinical score of how the mice stand from 0 to 5, 5 being death and 4 being significant disability. And you see in the vehicle control arm how that shoots straight up. And then, of course, the anti-CD20 antibody and then the significant activity that's seen with the Obexelimab surrogate here. This is a really compelling experiment. It's quite impressive what we see here. If you ran the trial 10 times, I don't know if it would look the same way all 10 times, but regardless, it's an active molecule. And then importantly, on the right, you see it's doing this without depletion. So just so you know, the Y-axis is the% of B cells of total lymphocytes. And it's sustained with obexelimab. So this is a non-depleting approach that's highly effective in the disease. So then, of course, the question is, knowing that, how much confidence can one have in the MS therapeutic hypothesis in the clinic? It looks great. It could work. Yeah. So the non-clinical data is there. We know mechanistically how potent and deeply B cell lineage is suppressed. We know how important the B cell-T cell interaction is in MS. And we know that anti-CD20s are quite effective in preventing relapse in the disease. So what we're doing is the classical MRI study in our MS population. And in this study, where you randomize versus placebo, it's a fairly quick readout because it's a 12-week primary endpoint. And the study is looking at cumulative new T1 Gd-enhancing lesions. And it's 90% power to show a 90% difference. Drugs that have shown a mid-80% to a mid-90% difference have virtually all gone on to then demonstrate activity in large randomized trials. So this is the gold standard. And it's a really good indication of drug activity. And if CD20s work, I don't see why CD19 wouldn't be a great concept. Others are actually thinking the same thing. We'll have this readout, the top line results in the third quarter of 2025. Then all patients end up on obexelimab for the final 12 weeks. We have a total of 24-week data that is looking at biomarkers, novel imaging techniques, building the scientific foundation as to why hitting B cells and specifically inhibiting B cells with a CD19 targeting agent could impact not just relapses, but potentially the underlying smoldering disease, sometimes referred to as the silent progression, which is the really large unmet need in this disease for patients. Their relapses are controlled, but they still continue to decline. There's now a clinical measure called PIRA, which is progression independent of relapse activity. We would like to consider, upon success in this study, including PIRA as a key secondary endpoint in the phase 3 program. And that would be the first time that's being done. We know from the CD20 data on Ocrevus specifically, when the two phase three studies were in a post-hoc manner, this is all retrospective, integrated in the PIRA clinical endpoint calculation was applied. It actually looks as if impacting B cells can help with PIRA. It's just that it was retrospective and it was a combined database. So if we did it prospectively, could that be a significant differentiation in addition to our convenient at-home dosing, the opportunity to pause and vaccinate? I think this could be a significant opportunity to help patients with MS. Now, there are two important things to observe, among other things with this trial, is the 12-week placebo versus Obexelimab, which is obvious. But then you have the 24-week where you're doing the switchover. And there's something potentially very interesting to learn there in terms of once you could do the crossover from placebo to Obexelimab, whether you see a catch-up effect. So can we. That's right. That's right. That's exactly it. Yeah. We have multiple secondary and exploratory endpoints that will be applied to both arms over time. And I think it'll be an interesting readout. And that's coming, so everyone knows it's. The 12-week top line primary endpoint, third quarter 2025. And then the other data sets add 12 weeks to that and a lot of analysis because this is involving biomarkers, a lot of imaging at special centers that are part of our program that will do this imaging. So this is the type of thing that we'll just keep giving data over time. So we'll probably have months of possible data releases. But the key point, you're going to get this potentially very interesting POC and MS before the phase 3. IgG4. So people understand the cadence of data. That's right. Okay. Very good. Let's talk about funding a little bit. So obviously, you did the IPO. You had the Series C. What are you funded to do? Obviously, you're funded through the IgG4 phase 3. MS, I assume if that hits in the studies we just talked about, then you need to think about additional sources of capital to do a large phase 3 in MS because that's a big undertaking. Can we just talk through that? Yeah. So we'll end the year with about $350 million in cash. And that takes us through the multiple sclerosis primary endpoint top line results. It takes us through the IgG4-RD top line results for phase three. It actually takes us all the way through the SLE to its primary endpoint. So all of those studies will read out based on this capital. Of course, if we move to phase three in either or both of SLE and MS, that will require additional capital down the road. To your point about MS, let's go back to lupus first. So we can prosecute a lupus randomized trial. I'm confident in that. And it's part of our rheumatology franchise. We have great relationships with rheumatologists that's building the IgG4-RD platform is there. Medically, commercially, it's all there. For MS, I think an organization of our size can be very effective commercially in MS also. The challenge will be the phase three program. These are large randomized trials that take time. So with that data set in hand from the top line results, it's an opportunity for the company to think about strategically how we might want to prosecute MS, what kind of partnering could be available, just to step back and strategically think about the company and what we do from that point forward with MS. Okay. And then just last one in the last 56 seconds, freedom to operate and the IP picture. Can we just do a quick rundown there? What's your runway on that aspect? Yeah. So freedom to operate is not a question at all. From how far of a runway, at a minimum, obviously, as a biologic in the U.S., we have the 12 years of exclusivity. In Europe, you can calculate up to 10 years. And in Japan, something similar. But then we have a whole variety of patents that are issued and patents that will be prosecuted over time, everything from use, clinical data, dosing, biomarkers that put us into the 2040s. Okay. So plenty of time. Yes. All right, Lonnie, thank you so much. Congratulations. Thanks again and happy holidays. You too. Thank you.