CTLA4 and neoplasm: Mechanistically, cadonilimab leverages concurrent PD−1 and CTLA−4 blockade to reinvigorate effector T−cell activity and augment T−cell priming while mitigating Treg−mediated suppression (28, 29); its tetravalent, Fc−silent architecture confers preferential avidity in dual−high PD−1/CTLA−4 tumor milieus and minimizes Fc−mediated toxicities (30), thereby supporting rational combinations with chemotherapy, anti−angiogenic agents, and local modalities (31–33).