Good morning, everyone. We will continue with the next session, which is Kiniksa Pharmaceuticals. Please note that this session will be audio only. With that, I'm pleased to turn it over to CEO Sanj Patel, who will kick it off with some introductory remarks. Sanj? Thanks, Paul. Good morning. Thanks obviously to Goldman Sachs for hosting us today. With me on the call are John Paolini, our Chief Medical Officer, Ross Moat, the ARCALYST General Manager and Head of Commercial, and Mark Ragosa, who's our Chief Financial Officer. As always, please note that we will be making forward-looking statements today that are subject to both risks and uncertainties. A review of these statements and risk factors are found under the heading of "Risk Factors" in our SEC filings. We are happy to have the opportunity today to discuss our recent approval and launch of ARCALYST in recurrent pericarditis, as well as our broader portfolio of immune modulating assets. On March 18th of this year, we announced the approval of ARCALYST as the first and only FDA-approved therapy for patients with recurrent pericarditis. ARCALYST in recurrent pericarditis became commercially available on April 1st, and we look forward to reporting our first full quarter of sales in our second quarter 2021 earnings report. I am also really excited today to announce today for the first time that the U.S. Patent and Trademark Office issued a patent today covering the use of ARCALYST in the treatment of recurrent pericarditis. This patent provides protection that extends into 2039, and that is 11 years beyond our orphan exclusivity. We also issued a press release this morning outlining the next steps for the development of mavrilimumab. We believe that our phase II data in non-mechanically ventilated patients with COVID-19 related ARDS suggest that mavrilimumab may be a best-in-class treatment option for these patients. As such, we are focused on the continued development of mavrilimumab for patients with COVID-19 related ARDS. We believe this strategy represents the fastest path to potential registration for mavrilimumab, and there remains a significant unmet need for this patient population. Our phase III trial in non-mechanically ventilated patients has enrolled over 400 patients, and we expect data in the first quarter of 2022. Turning to our other pipeline assets, we continue to execute on the development of vixarelimab and KPL-404, which is our anti-CD40 program. We're conducting a placebo-controlled phase II-B clinical trial of vixa in prurigo nodularis, and that's evaluating a range of once-monthly dose regimens via subcutaneous injection. We also recently reported positive phase I data for our potentially best-in-class CD40 program, and we plan to initiate a phase II proof of concept trial in rheumatoid arthritis. With those opening comments, I'll turn it back to you, Paul. Thank you, Sanj. Maybe we can kick off the Q&A with this morning's news. You did a press release update on your development plans for mavrilimumab. Can you maybe talk to us about the scope and nature of your FDA discussions and how you're prioritizing development of mavri and just how we should think about the sequence there? Yeah, absolutely. Maybe I'll start, then John, if you want to jump in, feel free to. Obviously, our discussions, as we said, with the FDA have been favorable, really across the range of potential indications for mavrilimumab. That was on the heels really of the positive phase II data that we had, in COVID-19 related ARDS, as well as the positive phase II data from our clinical trial in GCA. We also had discussions with them around the indication of RA. As we said in the press release this morning, we believe that the fastest potential path to registration is the COVID-related ARDS study. We've now enrolled over 400 patients, we're looking to enroll 600 patients as part of a phase III study, hopefully then obviously be part of a registration there. We're also pleased, though, that we had a nice delineation potentially for the GCA indication. There, what we said in the press release, that would potentially be just a single pivotal phase III study in GCA after that. As far as RA is concerned, obviously not something that this company would pursue itself, or certainly not on its own. It was really nice to have a potential regulatory path outlined, working with the FDA for potentially two phase III studies in rheumatoid arthritis. Again, that's probably not something we would take on our own. It's very nice to see the negotiations or discussions with the agency around mavrilimumab broadly and see the potential broad utility. That's really the order in which we'd progress things. Right. That's great progress on the regulatory front. Maybe diving into your two early or most advanced opportunities, specifically maybe starting with COVID here. You said earlier that you've enrolled about 400 patients with that aim of enrolling a total of approximately 600 patients. I guess, as you think about this relative to your earlier data, what would be considered a good result here? Either maybe you can comment, Sanj or John, possibly. John, why don't I let you maybe do a very brief recap on the phase II data that we saw and why we're so excited about the data in COVID, and then obviously move to the phase III, which as I said, is enrolling very well. Happy to do so. Thanks, Sanj. Good morning, Paul. Really a pleasure to speak with you. Yes, in April, we announced data from the phase II portion of our clinical trial, and that's a phase II/III seamless design, and that's in COVID-19 related ARDS. The results that we showed were from the non-mechanically ventilated patients, and this signifies a potential additive treatment effect of mavrilimumab, and that's on top of corticosteroids. What we saw was a 65% reduction in the risk of mechanical ventilation and death, and that was in a diverse patient population. When we look at mavrilimumab in the context of other treatments that are being evaluated, there is a real best-in-class potential here. We were particularly encouraged by the benefit-risk of GM-CSF receptor inhibition with mavrilimumab, given not only the fact that the treatment effect was sustained and was demonstrated throughout the 29-day observation period, and that was after only a single administration of drug. Also the fact that the safety profile demonstrated that mavrilimumab is well-tolerated to date. Yes, overall, we think that mavrilimumab is well-differentiated and potentially best in class in the space of COVID-19-related ARDS. We actually, as a side note, just recently had a scientific presentation of the data at the late-breaking session at the EULAR Congress just on Friday morning, Friday and Saturday morning. As we look at the phase III data going forward, specifically to your question as to what to look for, remembering that this is a seamless design, right? The first 120 patients that went through were in phase II, and then we continued to enroll directly into phase III with the same study design. What we're looking to do is essentially confirm and extend those findings from the phase II portion into that larger patient population. As you know, we've shared our data from phase II with the FDA, and so we're moving forward with our plans. We finalized the sample size, for example, to have the sample size be 600 patients. As Sanj mentioned, we have already 400 of those patients enrolled. Maybe one last word, which is about where do therapeutics fit in this situation where a lot of patients are being vaccinated. As you know, vaccination will always be the mainstay of the prevention paradigm. That's of critical importance. However, there really is an unmet need for COVID therapeutics as well, and specifically around these patients that are hospitalized with hypoxia that are at high risk of mechanical ventilation. As you know, these patients transition from when they first present, there's an early phase of a high viral replication load, and that's where antiviral therapies and the antibody cocktails have shown some benefit. It's really in that later phase of disease where there's that aberrant inflammatory response. That's what's causing the tissue response, the tissue damage, the thrombosis, the ARDS, and death. In that sense, the therapeutic focus has to be on the host response rather than on the virus itself. I think especially in this situation globally where we're seeing very, very high, almost uncontrolled viral transmission rates, for example, in Brazil and other parts of the world, those case rates are increasing the likelihood of variants that could evade the protective effects of vaccines and cocktails. I think that's the fact that mavrilimumab blocks this counterproductive inflammatory response in a way that's agnostic to the coronavirus sequence is of great importance. That's how we view the overall development scheme. Okay, great. Thanks for that, John. Your point on the existing opportunity in international geographies is well taken. With regard to your second key update in this morning's press release with development in GCA, I guess, the key thing here is that you can run a single phase III trial here. How do you think about executing on that and just what the timing on kicking that off potentially could be and just as you think about trial design here? Yeah. Obviously, we're really pleased with the discussions with the agency regarding that, and that was on the heels of the very positive phase II data that we had last year. Certainly, that's a path that we could follow. At this point, we're going to focus on getting the registration, hopefully, in COVID-19 related ARDS. Depending on that data, we'll delineate or describe next steps for the rest of the programs. It's certainly, as you say, a nice development that we've got a potential to single pivotal phase III study for registration in GCA. We'll provide an update in the future as far as on our timing around that. Okay, great. Thanks, Sanj. Maybe staying on the topic of GCA here, it seems like the clinical treatment paradigm is increasingly transitioning to biologics here. How do you compare the mavri data that you've had so far versus already approved products such as ACTEMRA in terms of efficacy and safety that we've seen so far? John, do you want to cover that? Sure, happy to do so. When we look at the data from the phase II study, we showed those data at ACR last November. The primary efficacy endpoint was time to first GCA flare at week 26, and we did that in the pooled population. It was a statistically significant 62% lower flare rate in mavrilimumab recipients compared to placebo. That was statistically significant, p-value of 0.0263. The secondary efficacy endpoint, if you look at the data from the other perspective, which is sustained remission at week 26 in all treated patients, that was 33.3 percentage points higher in mavrilimumab recipients. That means 83.2% of patients were in sustained remission at week 26 compared to just half of the placebo recipients. That was also actually highly statistically significant, p 0.0038. What you see there, that's in the pool population carries forward into the subgroups of patients. This is actually really important to the new onset and relapsing refractory cohorts. Mavrilimumab, in particular, seemed to do well in the relapsing refractory cohort, and that was the group of patients where biweekly tocilizumab struggled in their phase III pivotal registrational study, that was GiACTA. That 30.6 percentage point higher sustained remission rate in those relapsing refractory patients, it really compared quite favorably. Cross trial comparisons are always tricky, but it was only 20 percentage points with tocilizumab. Overall, of course, mavrilimumab being well-tolerated without drug-related serious adverse events, and the fact that mavrilimumab and placebo drug-related treatment emerging adverse event rates being similar, really speaks to the safety profile of the drug to date. When we put together this benefit risk profile, and we also showed, incidentally, as a side note, some recent data at the EULAR meetings just this past weekend showing that acute phase reactants such as C-reactive protein and sedimentation rate, those are actually still reliable for monitoring disease activity when patients are being treated with mavrilimumab. That actually could be an important differentiation element for clinicians because with tocilizumab, which of course, as you know, suppresses CRP production of the liver independent of the inflammatory state, makes monitoring of those biomarkers more challenging or less reliable. Taken as a whole, this upstream mechanism of mavrilimumab in this disease is very important to us, and it blocks the activity of GM-CSF and the downstream pathways. We think that in that sense, there's a real opportunity to potentially be best in class in this disease. Back over to you. Great. Thanks, John. How do you think about the opportunity for mavrilimumab in first- line treatment-naive patients versus a refractory or treatment-experienced patients? Will you be focusing on one population more? Does one make sense or is easier to focus on in terms of development? I think it will be both. From a prevalence perspective, if you look at giant cell arteritis patients, there are 75,000-150,000 patients in the U.S. alone, and those are essentially all being treated with corticosteroids first. 50%-70% of those end up with relapsing refractory disease, and they can't be tapered off the steroids, and they become steroid dependent. That can often be for years. There's a real need for those patients. When you look at the data and how patients are doing on standard of care, and that includes the fact that there's one drug already approved as an adjunct to steroid therapy, even still, only half the patients can remain in sustained remission on a yearly basis with standard of care. That's, I think, why we're excited about this mechanism, where by blocking GM-CSF pathway, you end up blocking two key immune pathways that are implicated in the disease, right? The Th1 and the Th17 pathway. That, I think is the key to the differentiation in addressing the underlying pathophysiology. In that sense, for the subgroups, what our data have shown to date is that mavrilimumab may actually offer differentiated treatment option really for both types of patients, relapsing refractory disease as well as those with new onset disease. Okay, great. That makes a ton of sense here. Maybe we can shift over to the commercial piece. You did mention you'll talk about your updated ARCALYST launch coming up here. Can you maybe provide us some preliminary commercial updates since your recent approval and launch earlier this year? Maybe some color on what physician feedback has been like. Absolutely. Ross is on the line and certainly can provide sort of an overview where we are. Just remind you, we had the approval in March. We launched the drug in April. We've obviously had the sales force in place by that time, about 27 reps with a cardiology focus, a lot of them with previous cardiology experience and relationships. We also had the MSL team in place for over two years, so that's really put us in good stead. Maybe Ross, you can provide a bit of color on the launch so far, and obviously, we'll look forward to reporting the Q2 sales sometime in August. Thanks, Sanj. Yeah, happy to do that. Paul, great to speak to you again. Maybe just to take a step back again, just as a reminder, we received the Breakthrough Therapy designation, also the Orphan Drug Designation, which led to a priority review and actually a slightly earlier approval versus the PDUFA date that got approval on the 18th of March. Now we have the commercial availability as of the 1st of April. We were very pleased with the very broad label that we achieved with the approval as well, which is the treatment and the reduction of risk of recurrence and recurrent pericarditis. Whilst we're not providing specific metrics right now, and we look forward to sharing information on our Q2 earnings report, we are very confident and happy with the commercial strategy that we put in place. We really spent a lot of time prior to the approval really understanding the marketplace and the patient journey. As Sanj said, we had the MSLs in the field for a good couple of years prior to the launch as well on disease awareness and really working with subject matter experts within the area. Really through market research and triangulation of claims data, we were able to put together a very focused and targeted strategy, and that's really what led to our strategy around just under 30 clinical sales specialists that we now have activated out in the field. We have very tenured sales professionals within that group, which is from cardiology experience or biologics or rare disease experience, and really focused on the targeted strategy. Which is really understanding where the patient throughput is, which centers are looking after those patients, and which healthcare professionals are treating the patients as well. With the team of just under 30 representatives in the field, we feel like we can cover around 70% of the total recurrent pericarditis patients out there across the U.S. In this early stage of launch, we're also really focused on a smaller group of that, which is around the 45% of recurrent pericarditis patients with a smaller number of accounts. Once we're comfortable with the uptake within those accounts, we'll expand out to the 70% there as well. We're really happy with the targeted approach that we have. We're also very focused on the 14,000 patients that fit into the refractory, the multiple relapsing, and the corticosteroid-dependent patients, which is highly representative of the very compelling data we have out of RHAPSODY. We're very focused on those groups. We believe there's a strong call to action with the physicians that may look after those particular patients as well. We're really focusing on mainly cardiologists, but also some rheumatologists that may look after those patients as well. To date, the physician feedback has been very positive. I mean, certainly they're looking for better treatment options. There was previously no approved drugs within this particular field for recurrent pericarditis. Our drugs at the moment are really systemic, and patients often cycle through those drugs and continue to break through. That's really where we're focused. We're happy with how receptive physicians are being to the data, and as we get out and reach more physicians, now we're out in the early stages of launch. Great. Thanks for that, Ross. Maybe as a follow-up, you guys received a very broad label here for ARCALYST without any meaningful restrictions as to regards to prior lines of therapy therefore. How is the shape of the label resonating with regard to physician feedback? I think with physician feedback, it's resonating very well, and I think also with payers as well. I mean, we were also really focused on the payer community in the pre-launch stage where we were doing early payer engagement with our payer team, who are now also fully operational out in the field. We had more than 150 payer engagements prior to the approval, which was really focused around recurrent pericarditis as a disease and the high-level topline results from the RHAPSODY data. Again, we're really focused on that customer group for us as well. Again, on the 14,000 patients, and ramping up after the approval and our engagements with those customer groups. Really focused on ensuring that we have minimal payer restrictions within the target population. I guess one important thing to note is really in line with our previous expectations. We know that there are viable reimbursement conditions ahead of when payers are actually establishing their full coverage policies via medical exceptions and processes. We see that as a viable route up until the full coverages and policies are in place, which we still expect that the majority of those will be within six months of the launch, and almost all of them within 12 months. Feeling confident that the payers will appreciate the specific benefits of ARCALYST as a targeted therapy and the first and only approved drug in this indication. We've also launched Kiniksa OneConnect as our patient services program, which is really pivotal in supporting patient access and affordability really throughout the patient journey on ARCALYST. Okay, great. Just you mentioned you'll get a decent chunk of the payer coverage in the next six months and mostly all of it in the next year, I guess. Just, I guess, as you engage in those discussions, should we think about maybe any sort of big chunks of progress with regard to payer coverage coming? Just how do you expect in terms of the major payers and major providers coming on board, I guess, in the time frames provided? Yeah, thank you. We really wait to see as those coverage policies start to come through, but as I mentioned, really feeling positive about the medical exceptions process prior to that happening. I guess in some way it helps us the fact that this drug has actually been available since 2008 in CAPS, then the approval at the end of 2020 in DIRA as well, another ultra-rare monogenic disease. Payers are really quite familiar with ARCALYST as a mechanism of action, and they have some familiarity around that. That may help during the medical exceptions process. We have a wait for the coverage policies to come into place, and we're actively engaging with payers both prior to the launch and now since launch. We've really kind of provided all of the value messaging on this disease and are excited about the future. Okay, great. Thanks for that, Ross. Maybe turning to the other parts of the pipeline here, we can talk about vixarelimab and how it fits into the PN treatment landscape and what you've been working on since your positive phase II data was previously published. Maybe as a follow-up to that, how do you think about that, the vixa data and development comparing to the nemolizumab phase II data, which was also previously announced a while back ago? Yeah. Maybe, John, I'll start with a few sort of broad level comments, and if you can just jump in with the positive phase II data, but obviously I want to remind everybody that there is currently no FDA-approved therapy for prurigo nodularis, and there are limited therapeutic options. The prevalence is around 300,000 in the United States alone, and we feel that this market could sustain multiple entrants, especially with different mechanisms. For right now, first-line therapy is typically topical steroids, and the second- line includes oral corticosteroids and UV phototherapy. The third-line therapy also involves systemic immunosuppressants such as methotrexate, cyclosporine, and thalidomide. It's obviously potentially great for patients that there could be a systemic therapy in development. Both vixa and nemo inhibit IL-31, which has been shown to inhibit pruritus, but vixarelimab also inhibits oncostatin M, which drives both fibrosis and hyperkeratosis, and potentially therefore translates into lesion improvement over time. We believe that the results we've had so far are very encouraging. We saw that from the phase II-A study in vixa, that both pruritus and nodule response are suggestive of the potential for the drug to make a positive impact on patients with prurigo nodularis. Obviously really pleased with that. As you say, we're enrolling in the phase II-B dose ranging study right now, and that trial's ongoing. Maybe, John, if you want to just focus on the phase II-A data as Paul asked about. Sure, happy to do so. The phase II-A data in prurigo nodularis showed the potential efficacy of this mechanism of OSMRβ inhibition. Specifically, the trial met the primary efficacy endpoint. That was a reduction in weekly average worst itch NRS from baseline to week eight. That was statistically significant within those receiving vixarelimab, with a nearly 70% reduction in median weekly average worst itch NRS that we gave. Importantly, when you think about the regulatory endpoint for clinical meaningfulness, which is a greater than four-point weekly average worst itch NRS reduction, that was also statistically significant, with the majority of vixarelimab recipients showing that. The results really extended beyond pruritus, and they went into the space of disease severity, which is important. 30.4% of vixarelimab recipients achieved a PN-IGA score 0 or 1, which is clear or almost clear at week eight versus placebo recipients. As a secondary efficacy endpoint, that was highly statistically significant. To your question of how do you put this into the competitive landscape with regard to the nemolizumab data. Of course, one should always approach cross-trial comparisons with some caution, but there are a few caveats to keep in mind when looking at the differences in the two study designs, and then we can talk about the results. Obviously, precision around the point estimates. The nemo study was bigger with 70 patients versus vixarelimab at 49, and slight differences in the patient population where the nemolizumab study was run in Germany and vixarelimab primarily in the U.S. There are some subtle differences in how the disease is characterized or defined. Mechanistically, I think this is where it gets really interesting, where nemolizumab is blocking IL-31 only, whereas vixarelimab is blocking not only IL-31 but also, as Sanj mentioned, oncostatin M inhibition. We know that oncostatin M drives fibrosis and hyperkeratosis. When we put that together in terms of those results with vixarelimab, and the fact that in addition to the strong antipruritic response, seeing that robust disease severity benefit and lesion improvement, and there's an interesting insight there. It's not just that the PN-IGA at week eight and the delta was nearly 1/3 of patients having that response versus only about 10.6% in the nemolizumab patients. What it means is that these patients were seeing that effect at week eight was actually of similar magnitude and also statistically significant at week six. There was curve separation as early as week four in that phase II-A study of ours. Whereas the nemo response was slower and had a smaller magnitude of response. Of course, we have to replicate these findings in the phase II-B study, and we have a 16-week study ongoing in order to do that. At this point, the data that we have in hand speak to why we believe at this time that vixarelimab could in fact be potentially best-in-class asset in this space. Okay, great. Thanks for that, John. In addition to your focus with vixa in terms of developing it for PN, you have a lot of other things going on here, which include 404. Can you maybe talk about some of the proof of concept data that you have there and how you think about 404's role in T-cell dependent and B-cell mediated opportunities? Maybe, John, if I make a couple comments, maybe you can jump in. First of all, foremost, we're really excited about this program, and I think I've said to you, Paul, in the past, a lot of that excitement also comes around from the fact that we own the vast majority of the economics for this program, and we really believe it's got a potential to be a very strong value driver for the future of the company. We recently did report final data from the phase I trial, and John can review that, and that was very, very encouraging. They really confirm and extend the findings that we found from the previously reported lower dose cohorts, which we reported in November of last year. The data continues to reinforce our confidence in 404 as a potential best-in-class treatment option and really support the optionality for studying chronic dosing in patients with both subcutaneous and/or intravenous administration. Based on that, we plan to continue the development of that program, potentially now in a phase II proof of concept study in rheumatoid arthritis patients. Maybe, John, a few additional details on the data and then really the broad potential applicability of this program. Yeah. Thank you, Sanj. Yes, the phase I study with 404, that was a healthy volunteer study, single ascending dose, but it was still a randomized double-blind placebo control. What we saw, of course, were dose-dependent increases in concentrations across cohorts and with safety and PK being the primary endpoints, of course, the safety showed dose limiting safety findings, KPL-404 was well-tolerated, no serious adverse events. Speaking specifically to the data, back in November, we reported 3 mg/kg IV data. In that context, what we saw with that dose level, single dose, was that receptor occupancy and suppression of the T-cell dependent antibody response after KLH challenge, we saw all those through day 29. In fact, there was even a complete suppression of the memory TDAR response when we rechallenged with antigen at day 29 with just the drug levels that were still remaining in circulation at the time from the prior administration. The new data that we just reported are exciting because the higher dose data at 10 mg/kg IV extended the full receptor occupancy through at least day 71 and gave complete suppression of TDAR after the KLH challenge and even rechallenge through day 57. I think the most exciting piece of data really speaks to the optionality of subcutaneous dosing going forward into patients. There we used a 5 mg/kg subcutaneous dose, which actually could be practically administered going forward. That showed full receptor occupancy through day 43 and suppression of TDAR after KLH challenge through at least day 29, which is when we stopped measuring. Now, another way of looking at the data is to look at anti-drug antibodies, and this is particularly useful in a competitive landscape. We saw suppression of anti-drug antibodies for at least 57 days through 10 mg/kg IV. That itself is an independent indicator of target engagement and pharmacodynamics. Now armed with these single-dose data in healthy volunteers, we've now set the stage for that longer duration exposure in patients going forward, and we can talk about that study if you like. Okay, great. The sub-Q optionality, I think, is really attractive here. Maybe you can elaborate a little bit more on the phase II plans here in RA and just how you think about maybe identifying the population. Go ahead, John. Sure. Yeah, sure. Happy to do that. This trial is essentially a proof of concept study with a PK lead-in. What we did was we selected rheumatoid arthritis patient population, not so much because this is our broader plan, but rather as in a focused way for this particular study, trying to characterize the molecule as well as to look for evidence of early signal of efficacy, if you will. This is a well-characterized autoimmune disease, and there are decades of published clinical data across diverse mechanistic classes. In that sense, we can get an objective evaluation using established endpoints on a relatively small number of patients over a relatively brief period of time. The way we're approaching the study, and of course, more details to come, but the first part of the study evaluates the safety and pharmacokinetics of KPL-404 in subcutaneous administration. Essentially, we're bridging from the single-dose healthy volunteer data into chronic dosing in patients. From there, we go up the dose escalation after the PK lead-in with a 12-week proof of concept portion of the study. There we can use those rheumatoid arthritis endpoints and look for essentially the maximum horsepower of the mechanism and of the drug. Of course, more details to come as we file in ClinicalTrials.gov at a later date. Maybe one last point, which is that with this study design, it really gives us optionality again to do proof of concept studies in other diseases if we want, using those data in hand. In that sense, this planned study is important not only to characterize chronic administration of 404 in patient populations in general, but it provides that option to evaluate the therapeutic potential of KPL-404 across a range of other autoimmune diseases with the pathologies that we believe have been mediated by the CD40 and CD154/CD40 ligand pathway. Of course, you know that the literature is rich with a number of external proof of concept studies there. Maybe I'll pause there. Great. Thanks for that. We're coming up on time here. We have maybe time for one more question, which is, Sanj, I sense your palpable enthusiasm for this program here and just can you think about or help us understand how you think about the additional autoimmune opportunities for 404 here and what might make sense for future development? Definitely palpable, the energy, and a lot of that is around the economics. As John said, we're going to use this phase II proof of concept study to really help guide our decisions, and we really think this could be a best-in-class molecule that we practically own. There are a number of autoimmune diseases that are out there, and the nice part about this program is there's been external validation in a number of different indications, Sjögren's, et cetera, and other areas. We think RA is the right one as far as proof of concept, somewhat of a proxy, as you will. We definitely look forward to updating folks on next steps, and we'd like to make them as concurrent as possible, certainly as far as other indications. More to come, but it's a very, very exciting program. Great. We'll have to end that on that note because we're up on time here. Thank you very much to Sanj and the team for joining us today. Cheers. Thanks, Paul. Thanks, everybody Thank you. Thanks so much. Bye now.