In AMLs where FLT3-activating mutations, and in particular FLT3-ITD, are present, FLT3 is a critical therapeutic target.41,42 There are currently several FLT3 inhibitors in clinical use but achieving to long-term remission when it is used as a single agent is challenging.27,42,43FLT3-ITD is a secondary genetic event in in our patient-derived NUP98-r AML and its signaling may also cooperate via STAT5 with MLL–Menin complexes in regulating gene expression.27 Here we showed that Menin inhibition suppresses FLT3-ITD expression and also increases this AML subtype susceptibility to FLT3 inhibitors. The gene discussed is KMT2A; the disease is acute myeloid leukemia.