Acute myeloid leukemia (AML) is one of blood cancer categories characterized by the clonal growth of immature hematopoietic stem cells or progenitor cells. Genetic mutations of fms-like tyrosine kinase 3 (FLT3) such as ITD; Intrernal Tandem Duplication and TKD; Tyrosine Kinase Domain mutations are known to be the most frequently observed in AML patients. The mutant FLT3 is constitutively activated in a ligand-independent manner and causes the abnormal growth. Gilteritinib was synthesized in the ALK inhibitor research and developed for the treatment of FLT3 mutation-positive AML because of its FLT3 inhibitory effects found in the drug discovery studies. Gilteritinib was approved two years ago for the first drug for the treatment of relapsed or refractory AML with FLT3 mutation in Japan and the U.S. after a global phase III study. This presentation will highlight the pathogenesis of AML, the role of FLT3 in AML, and non-clinical pharmacological data on Gilteritinib.