Of particular interest are the activating mutations in the FLT3 gene, such as internal tandem duplication (FLT3-ITD) or D835-activating point mutations (FLT3-TKD), which lead to the overexpression or constitutive activation of the kinase, and occur in about 30% of AML cases [5]. This evidence concerns the gene FLT3 and acute myeloid leukemia.