In marked contrast, neither of the FLT3 TKD point mutations decreased the cellular sensitivity to the dual FLT3-ITD/PIM inhibitor SEL24-B489 (Figure 2), underscoring the role of PIM kinases as key FLT3-signaling effectors and circumstantiating the concept of dual PIM-FLT3-ITD inhibition in AML targeted therapy. This evidence concerns the gene FLT3 and acute myeloid leukemia.