Not only the response to anti‐PD‐1 therapy correlates with the levels of tumor‐associated NK cells,[10] depletion of NK cells also compromises the improved survival by anti‐PD‐L1 therapy in tumor‐bearing mice,[11] and activated human NK cells could sensitize tumor cells to PD‐1 blockade therapy in vitro.[12] Despite the above‐mentioned accumulating evidence of NK cell helper functions in supporting the CD8+ T cell antitumor response, the underlying molecular mechanisms remain poorly defined. The gene discussed is CD274; the disease is neoplasm.