And as was mentioned earlier that includes not just B-cells that you might be able to take out with a CD20 T-cell engager, but also B-cells you might be able to take out with a CD38 or a combination of the two. So, our landscape is just really, really broad here in terms of what we might be able to do with a portfolio of T-cell engagers in autoimmune disease. And we think we’re in a €“ we have the potential to be in a real leadership position here. And we think our safety is perhaps the most important differentiating factor. Mary Beth, did you want to add to that?
Mary Beth Harler: Yes. No, thank you. I think, those are absolutely critical comments, right. We expect these initial studies in patients this year to inform on which development programs make the most sense for this particular mechanism, right. And I think for those of you who have been in the autoimmune space in the past, right, there is a lengthy list of potential diseases here. We could also think about in addition to the anti-CD20s and where the CAR-Ts are currently going in autoimmune disease, we could even contemplate perhaps, where the FcRns are going. So there is, as Fred indicated, there is a very broad range of opportunities. And I will come back to his last remark, right. We not only have a very active molecule, but we think we’ve got a safety profile that will define the bar for this new class of therapies around T cell engagers in autoimmunity. So it’s an exciting place to be.
Greg Harrison: Great. Great, that’s super helpful. Maybe just one other if I can a much narrower question. On IGM-8444 the biomarker data that you discussed looks encouraging, you are seeing in almost every patient. How would you expect that to correlate into a clinical response?
Fred Schwarzer: Chris, do you want to take that one?
Chris Takimoto: Yes. No, great question, Greg. So, obviously this is something that we’re looking at very carefully. I think though, when you first €“ when you think about caspase-3, it’s a cell death biomarker, it really is an indication of how well your agent is engaging the target and target pathway. And so, the most important information is that it’s telling us that the signal of engagement in modulating the extrinsic apoptotic product pathway is quite strong at 10 milligrams per kilogram. We’re obviously looking at how this correlates with other clinical parameters. And again, the data are still very early, so we can’t really draw any direct conclusions there. But again, in terms of a pharmacodynamic marker, we think it’s very, very positive and very informative.
Greg Harrison: Great. That helpful. Thanks again for taking the questions and congrats again on all the progress.
Fred Schwarzer: Thank you.
Chris Takimoto: Yes.
Operator: Thank you. One moment for our next question. And our next question is from Michael Schmidt with Guggenheim. Your line is open.
Michael Schmidt: Hey guys, thanks for taking my questions. I had two. Perhaps so, one on IGM-8444, you updated us on your combination arm with birinapant as well, it seems to be progressing in dose escalation. Could you just remind us which types of patients are likely to respond to that particular combination? Just curious how you think about that. And then on CD20 obviously, a large commercial opportunity across a huge number of indications here. Does that shift in development strategy affect how you think about partnerships for this program that, perhaps could maximize the opportunity if you have a large company on board for that? Thanks so much.
