Abstract: Acute myeloid leukemia(AML) is a heterogeneous disease characterized by diversity in molecular pathogenesis and clinical manifestations. Studies have shown that AML involves multiple gene fusion and mutations, including gene fusion of transcription factors(such as PML-RARA and RUNX1-RUNX1T1), mutations of key signaling molecules(such as NPM1 and FLT3) and epigenetic modifiers(such as IDH1 and IDH2). These genomics changes in AML usually have clear correlation with the clinical diagnosis and prognosis of the patients, which are widely used to guide the clinical treatment and indicate the prognosis of AML. However, there are still many AML patients lacking known biomarkers, and some new genetic mutations are constantly emerging. Elucidating the functionality of gene subtypes in AML will contribute to the development of therapeutic drugs. This article elaborate on some known functional genotyping in AML, the current clinical treatment of AML, and review the progress of drug therapy targeting specific AML subtypes. It is expected to provide a new reference for the development of therapeutic drugs for new AML gene subtypes.