An increased EGFR expression, in turn, leads to an increased glutamate concentration in the TME (Fig. 2), which promotes glioma cells migration via phosphorylation of the COOH terminal (carboxyl-terminus) of GluN2B (glutamate (NMDA) receptor subunit epsilon-2), resulting in increased glutamate-NMDAR-signaling [12]. This evidence concerns the gene EGFR and glioma.