Within tumor‐specific immune responses, PD‐L1 primarily suppresses cytotoxic T cell activity in the TME by binding PD‐1 receptors,[94] while cytotoxic T‐lymphocyte associated protein 4 (CTLA‐4) inhibits early T cell activation through competitive B7 family of costimulatory molecules (B7) binding.[95] These checkpoints synergistically establish profound immunosuppression.[96] Dual blockade of PD‐L1/PD‐1 and CTLA‐4/B7 axes thus reactivates exhausted T cells and facilitates initial priming, enhancing antitumor efficacy.[97, 98] Leveraging this strategy, Qiao et al. This evidence concerns the gene CD80 and neoplasm.