While the complexity of the pathogenesis and heterogeneity of AML is appreciated, the presence in a subset of patients of mutated FLT3, the ITD variant of which has been shown in mouse bone marrow transplantation assays to cause a rapidly lethal myeloproliferative disease in the absence of any significant block in granulocyte lineage cell differentiation [27], would suggest the availability of a key therapeutic target that contributes strongly to the AML phenotype in these patients. The gene discussed is FLT3; the disease is acute myeloid leukemia.