Well, the next chapter is in many ways, what we’ve talked about, which is the bi-specifics and the DARTs and the ADCs that are targeting these variety of different antigen targets on the surface of myeloid blasts. So we alluded to CD33 and CD123, but there are others. So CL1, FlT3, CD70. So, and- and in fact, I- I forgot to mention that not only antibody-drug conjugates, and BiTEs, but also naked antibodies seem to have a lot of legs still the most advanced in clinical trials...
Well, the next chapter is in many ways, what we’ve talked about, which is the bi-specifics and the DARTs and the ADCs that are targeting these variety of different antigen targets on the surface of myeloid blasts. So we alluded to CD33 and CD123, but there are others. So CL1, FlT3, CD70. So, and- and in fact, I- I forgot to mention that not only antibody-drug conjugates, and BiTEs, but also naked antibodies seem to have a lot of legs still the most advanced in clinical trials. And perhaps the most promising, currently is CD47 antibody magrolimab, which blocks the CD47 antigen. The so-called “don’t eat me signal” and allows macrophages to come along and kill off malignant cells. In combination with a hypomethylating agents, azacitidine, it seems to have significant activity in myeloid malignancies and in a particularly troublesome group of patients, P53 mutated patients, at least in a very small group, it seems to show a promise inkling of activity. So that -that is exciting and intriguing. And we’ll have to see where that goes.