Activating mutations in FLT3, such as internal tandem duplications (ITDs) in the juxtamembrane domain of the FLT3 receptor and tyrosine kinase domain (TKD) mutations, occur in approximately 30% of adults and elderly patients with AML and induce ligand-independent proliferation stemming from constitutive activation of the FLT3 receptor [3–5]. This evidence concerns the gene FLT3 and acute myeloid leukemia.