While immune checkpoint inhibitors (ICIs) targeting the programmed death-1 (PD-1)/PD-L1 axis have transformed the treatment of various solid tumors, their effectiveness in gliomas is limited (4–6).This therapeutic resistance originates from the unique immunosuppressive tumor microenvironment (TME) of gliomas, primarily characterized by immune cell infiltration including tumor-associated macrophages (TAMs), regulatory T cells (Tregs), and myeloid-derived suppressor cells (MDSCs). The gene discussed is CD274; the disease is glioma.