KMT2A and leukemia: This suggests that in contrast to FLT3 activating mutations or amplifications, FLT3 signaling resulting from overexpression of wild type FLT3 may not cause a proliferative advantage to MLL-rearranged leukemias in vivo; this is consistent with our findings that Flt3 deficiency does not delay MLL-rearranged leukemias.