Previous studies indicated that GBM patients exhibit resistance to immune checkpoint inhibitors (ICIs) due to the low mutation rate, the PTEN-deficient immunosuppressive microenvironment, infiltration by myeloid-derived suppressor cells (including TAMs, prominent players in brain cancers), and activation of tumor stromal cells (56, 57), indicating that knockdown of HSPA7 may enhance the efficacy of ICIs such as PD1 inhibitors in GBM. This evidence concerns the gene HSPA7 and neoplasm.