Beyond Cell Cycle Control: CDKN2A Loss Orchestrates NAD (+) Metabolic Plasticity and NAMPT Inhibitor Sensitivity in Glioblastoma

While CDKN2A loss is classically associated with cell cycle deregulation through the p16-Cdk4-Rb axis, our findings suggest an additional layer of metabolic vulnerability arising from altered NAD homeostasis in CDKN2A -deleted glioblastoma, revealing a previously unrecognized metabolic-genetic interface for rationally revisiting NAD (+) targeting strategies, moving beyond the broad inhibition approaches.