Scott Wolchko: Sure. I mean, I can talk to at a high level, I mean, there is three different programs that we have looked at primarily with respect to, let’s just call it, sort of an ADR platform. There is the potential to target 4-1BB expressing alloreactive immune cells, which happened to include both T and NK cells, importantly. And so, with 4-1BB, we certainly think we are €“ have the potential to address the complement of host immune cells that may mitigate rejection. And importantly, with that specific ADR technology that sends a potentiation signal to the cell as well, which we also think is important and differentiated from the passive approaches. The other approaches we have looked at are certainly CD38 on developing a CAR against CD38, we think that’s a very interesting approach, again, similar to the 4-1BB strategy, CD38 will take out or be able to defend the cell against activated allo, allo-activated cells, whether they be NK cells or T cells expressing CD38.
So we think that’s a similar type of strategy that we also like and obviously in the format of a CAR can activate and potentiate the cell a differentiated approach. The third strategy, I’ll let Bob talk about that is the CD54 CD58 knockout and we think that’s an interesting approach. So we think it’s primarily interesting in the context of the cell defending itself against an NK-cell therapy attack, which we do not think is sort of a prevalent mechanism of rejection. And importantly, it doesn’t provide an activating signal in its current form as well.
Bob Valamehr: That’s right Scott. Just to follow-up what Scott is mentioning, 54/58 knockout comes into play when knocking out B2M and that was an experiment that we worked with our collaborator, , as the solution for our B2M knockout strategy where we feel strategies such as CD47 overexpression or HLAE come up short. So in this perspective, 54/58 does play a role, but just to echo what Scott said earlier about ADR and our current focus is I really, really believe as Scott outlined, ADR is a true replacement of Cy/Flu. It helps protect against an allorejection. It helps potentiate and also create space. And these are the steps that we believe Cy/Flu brings to the table. And so we feel that ADR is the focus, but other strategies are there and we will continue to pursue our self program in such a manner.
Operator: Thank you. Our next question comes from Michael Yee with Jefferies. Your line is open.
Unidentified Analyst: Hi, good afternoon. It’s on for Mike. Just two questions, one on the actual pipeline and the second on financials. On the pipeline, can you kind of let us know what the bar is or what the expectations are on efficacy for both 576 and 819, like, what are you looking for in terms of the bar? And then secondly, on the financials, is the $12 million to $16 million going to be just a one-time incurring expense for Q1 and then we expect expenses overall to drop, talk a little bit about that and the potential for combination or sequencing of therapies?
Scott Wolchko: Yes. With respect to the 576 program and the bar we are looking for, obviously, it’s a competitive landscape. And we are trying to develop a differentiated therapy. Part of the differentiation that we are looking to seek is essentially a cellular therapy that can be given in combination with monoclonal antibody therapy, which is used across multiple lines in treating patients with multiple myeloma. The monoclonal CD38 targeted monoclonal antibody therapy may serve as a conditioning agent as well. And so we do believe that we can, number one, develop a cell therapy that can plug into standard of care regimen. Number two, because it is an off-the-shelf cell therapy, potentially reach patients earlier and in an outpatient setting.
