Collectively, these data suggest that downregulation of FLT3-ITD, and crucially, reductions in STAT5A phosphorylation and gene activation are more sensitive to perturbations of MLL-fusion-mediated gene activation and are the main source of inhibitor effects on leukemia cell survival when expression of the canonical MLL-r proliferation mediators HOXA9 and MEIS1 are not substantially affected (model, Figure 7—figure supplement 1G). This evidence concerns the gene KMT2A and leukemia.