Cancer cells are also found to induce PD-L1 secretion by activating various receptors [19], such as Toll-like receptor (TLR) [20], epidermal growth factor receptor (EGFR) [21], interferon alpha receptor (IFNAR) [22], and interferon gamma receptor (IFNGR) [23], and while a blockade of PD-1/PD-L1 immune checkpoints has yielded significant improvements in several kinds of tumors [24,25], it is not so with GBM. This evidence concerns the gene PDCD1 and glioblastoma.