Acute myeloblastic leukemia (AML) is a biologically complex and clinically aggressive hematologic malignancy. The article summarizes genomic and functional therapeutic biomarkers used in AML therapy. Targeted therapies include BCL-2 inhibitors, such as venetoclax, which use BH3 profiling to identify BCL-2 dependence of AML cells. Epigenetic treatments include DOT1L (pinometostat), BRD4/BET (FT-1101), and LSD1 (iadademstat) inhibitors. Iadademstat in combination with azacitidine in the phase 2 trial achieved a response in 81% of patients, of which 52% were in complete remission (CR/CRi), and 82% of evaluable CR/CRi patients were negative for minimal residual disease by cytometry. Other biomarkers such as IDH, FLT3 and menin inhibitors enable precision medicine in AML. Challenges include the heterogeneity of AML cells and the need for combination therapies.[1][2][5]