Drug sensitivity profiling revealed high-risk AML patients exhibited increased vulnerability to inhibitors targeting key pathways: cell cycle regulators (e.g., CDK4/6 inhibitors), apoptosis inducers (e.g., BCL-2 inhibitors), and epigenetic modulators (e.g., HDAC inhibitors), with additional efficacy against DNA damage repair and tyrosine kinase pathways, suggesting dependencies on cell cycle dysregulation, apoptosis resistance, and epigenetic remodeling (Supplementary Figure S8, Supplementary Table 11). The gene discussed is BCL2; the disease is acute myeloid leukemia.