FLT3 mutations occur in about 1/3 of AML patients, resulting in constitutive activation of FLT3 and its downstream signaling pathways including PI3K/AKT, STAT5, and MAPK, leading to uncontrolled cell growth and reduced apoptosis.1,2 There are two types of FLT3 mutations: internal tandem duplication mutations in the juxta-membrane domain (FLT3/ITD) and point mutations in the tyrosine kinase domain (FLT3/KD). This evidence concerns the gene FLT3 and acute myeloid leukemia.