Researchers from Rutgers and international collaborators identified a molecular mechanism that underlies therapy resistance in acute myeloid leukemia (AML), offering new targets to overcome relapse after frontline treatments such as venetoclax. The study dissects pathways that allow AML cells to survive targeted apoptosis and rewire metabolism under drug pressure. Authors detail preclinical validation and nominate candidate nodes for combination therapy to resensitize resistant clones. The findings add mechanistic clarity to a major clinical problem and set up translational efforts to test rational combinations in clinical trials.