The most commonly found genetic mutations that contributed to the development of AML are tumor protein 53 (TP53), internal tandem duplication of FMS-like tyrosine kinase 3 (FLT3-ITD), nucleophosmin 1 (NPM1), and CCAAT/enhancer-binding protein alpha (CEBPA) [7]. This evidence concerns the gene FLT3 and acute myeloid leukemia.