The TME of GBM may partly explain the suboptimal outcomes observed, as a study has shown that the clinical response to anti-PD-1 immunotherapy in GBM is linked to specific genetic alterations, immune-related expression profiles, and the degree of immune cell infiltration, which collectively reflect the tumor’s clonal evolution and adaptive immune landscape during treatment (22, 30). The gene discussed is PDCD1; the disease is neoplasm.