GBM iGluRs may be stimulated either via neuron–tumor synapses or by glutamate released in an autocrine fashion by tumor cells through the cystine–glutamate antiporter (xCT) (Takano et al. (2001) [292]) or by neighboring reactive astrocytes (Sin et al. (2013) [107]). This evidence concerns the gene SLC7A11 and neoplasm.