Multiple effects of GluRs have been found in GBM: (i) the phosphorylation of transcription factor CREB followed by NMDAR activation is responsible for the promotion of GBM survival and migration, as well as the increase in radiosensitivity through inhibiting the repairment of the DNA double-strand break (DSB) [40]; (ii) AMPARs mediate the Ca2+-dependent activation of the AKT/PKB signaling pathway, stimulating tumor growth and invasion [41,42,43,44]; (iii) different subtypes of mGluRs induce opposite effects on GBM. The gene discussed is AKT1; the disease is glioblastoma.