How do you define a target? So that's always the first question. If your goal is to develop new treatments and any types of immunotherapies, anyways, so then the first question is always, what's a good target? And there's a lot of agreement in the field. Our own group has come up with a definition a couple of years ago, and we said we want the target, if possible, we want it to be expressed only on the tumor cells. That's number one. If possible, no expression on any normal tissues. And so that was number two. And then we said among patients with a given disease, such as multiple myeloma, we would like the target to be expressed on all their tumor cells, not just on 50% of the tumor cells or even 90% of the tumor cells, but on 100% of the tumor cells, if possible. We're talking about an ideal target. So an ideal target would be expressed on all of the tumor cells in a patient. And you would find high expression, relatively high expression on every single tumor cell, because that's one way of avoiding tumor escape. If you manage to kill the last cell because of the fact that it expresses, all of the cells express the target, then you'll be able to achieve a cure. It's very simple. So that's number three. You want homogeneous, strong expression on all the tumor cells, if possible. And then we said it would be good if the target had a function in tumor cells, because none of these were developed. The targets are not there because they're targets. They're there because they fulfill a function. If they do fulfill a function in tumor development and growth, then it will be much harder for the tumor cell to get rid of the target and to evade the immune response. If it has a central, important function for the myeloma cell, then the myeloma cell won't be able to afford the loss of the antigen easily. So we thought that that's an important criterion. And the last one that I would like to mention is the fact, and that's what we said even before BCMA was ever mentioned. We said it's probably not a great thing if you have a lot of soluble protein, a lot of the soluble version of the target protein in your blood, in your bone marrow, everywhere, because that will inhibit the effect or function of the CAR T cell, for example. If you have a lot of soluble protein floating around that's not bound to a tumor cell, it's just floating around in your blood, in the bone marrow, then the CAR T cells will bind to that soluble protein, let's say soluble BCMA, for example, instead of the BCMA present on the tumor cells. And that will inhibit the function of your CAR T cells. So we said that was the fifth criterion where we said that's probably not ideal. And again, we're talking about an ideal tumor antigen. I'm not even sure whether there is an ideal tumor antigen for any of the malignancies we're talking about. But for an ideal tumor antigen you would probably like to avoid massive amounts of soluble target in your blood and bone marrow and so forth. Are there any other cells besides the myeloma cell that the target should be expressed on? The target should be expressed on myeloma precursors. You could call them myeloma stem cells, myeloma progenitors, myeloma precursor cells, myeloma propagating cells. It's all different names for the same thing. And that's something, a certain population of myeloma cells that nurtures the development of new myeloma cells. And that's at least partially responsible for relapses after an initial response to the treatment. So you have this treatment resistant, proliferative, dormant cell population somewhere in your body, most likely in the bone marrow niche. And then these cells will be reactivated and repopulate the bulk of tumor cells once you suffer a relapse. So we said, don't we need to address this population as well? Not just the bulk of tumor cells, but the root of all evil. The cells where all the other cells come from. And that's what we tried to address when we developed our CD229 CAR T cells. Because then we found out that in contrast, for example, to BCMA and other tumor antigens, the CD229 is not only expressed or present on the bulk of myeloma cells, but also on the myeloma precursor cells. So that was the first finding. And then we found out that if you use CD229 CAR T cells, you will not only kill almost all, if not all, of your myeloma cells, but you'll also kill the myeloma precursor cells at the same time using the same treatment. And that's something I think that retrospectively, I think that that was a very important finding. So I would add this to all the criteria I mentioned before. For an ideal target, we think it would be good for the target to be expressed on cancer precursor cells as well. So that you target not only the bulk of tumor cells, but everything at the same time.