FLT3 internal tandem duplications (FLT3-ITDs) are seen in approximately 25–30% of patients with de novo AML, while an additional 5–10% of patients harbor point mutations in tyrosine kinase domain (TKD) that results in constitutive tyrosine kinase signaling (Fig. 2) [54, 55]. This evidence concerns the gene FLT3 and acute myeloid leukemia.