CD8A and neoplasm: ThePROTAC degrader NP1192 disrupts ac4C modification of HIF-1αmRNA, suppressing PD-L1 upregulation and reversing immunosuppression.In syngeneic models, NP1192 combined with anti-PD-L1 therapy synergisticallyinhibits tumor growth, reduces lactate production, and enhances CD8+ effector T cell function while decreasing the number of exhaustedT cells.