As a typical “cold tumor”, the immune microenvironment of glioblastoma is replete with inhibitory cytokines, numerous immunosuppressive cells, and insufficient effective T cells.[43] Moreover, tumor cells often evade immune surveillance by highly expressing molecules such as PD‐L1 and IDO.[44, 45] Existing studies have shown that while exerting cytotoxic effects, TMZ can induce immunogenic cell death of tumor cells to release tumor‐associated antigens (such as ATP and HMGB1),[46] creating conditions for the efficacy of immune checkpoint inhibitors. This evidence concerns the gene CD274 and neoplasm.