Mutations of Nucleophosmin-1 (NPM1) and activating mutations in FMS-like tyrosine kinase 3 (FLT3), including internal tandem duplications (ITDs) and tyrosine kinase domain (TKD) mutations represent the most frequent genetic aberrations in AML [1,3,4,5]. This evidence concerns the gene FLT3 and acute myeloid leukemia.