Glutamate exerts its tumorigenic effects via autocrine (activating glutamate receptors on GBM cells themselves) and paracrine (on adjacent astrocytes and neurons) stimuli and through the activation of AMPAR lacking GluR2, increasing Ca2+ influx and triggering growth-related MAPK and Akt pathways (Figure 2) [88,89]. The gene discussed is AKT1; the disease is glioblastoma.