This poor prognosis stems from GBM’s profound intratumoral heterogeneity, diffuse infiltration, rapid acquisition of therapy resistance, and a highly immunosuppressive tumor microenvironment characterized by abundant M2-like macrophages, regulatory T cells, elevated programmed death-ligand 1 (PD-L1), and immunosuppressive cytokines, which collectively limit the efficacy of conventional immunotherapies such as cytotoxic T-lymphocyte-associated protein 4 (CTLA-4)/programmed death-1 (PD-1) inhibitors. Here, CTLA4 is linked to glioblastoma.