With the advance of next-generation sequencing, we have gained more understanding of the molecular pathogenesis of AML, which leads to the application of several targeted therapies to inhibit crucial mutations and overexpression of oncogene for leukemia progression, such as FLT3, IDH1/IDH2, and BCL2 (5–8). The gene discussed is FLT3; the disease is acute myeloid leukemia.