For example, (1) GBM patients with PTEN mutation have no significant response to anti-PD-1 (Programmed cell death 1) immunotherapy due to the mutation-induced changes in the immune microenvironment (25); (2) patients with PTEN-negative GBM have a shorter survival time after initiation of bevacizumab than those with PTEN-positive GBM (26); (3) loss of PTEN leads to clinical resistance to PI3Kα inhibitors (27); (4) fibroblast growth factor receptor 2-mediated phosphorylation of PTEN at tyrosine 240 contributes to the radioresistance of glioma (28). This evidence concerns the gene PDCD1 and glioma.