The last 2 decades have seen significant progress in identifying diverse genetic driver mutations in AML and in developing therapies directed against those mutations, such as inhibitors of FLT3 (FMS-related tyrosine kinase 3), IDH1/IDH2 (Isocitrate dehydogenase 1/2), BCL-2, and MENIN, and epigenetic modifiers.2 The gene discussed is FLT3; the disease is acute myeloid leukemia.