Furthermore, the re-uptake of glutamate from the extracellular space is also impaired in glioma tissue, as expression of glutamate transporter 1 (GLT-1), also known as excitatory amino acid transporter 2 (EAAT2), is downregulated, or carriers are mislocalized, and therefore sodium-dependent re-uptake of glutamate is reduced [37,45,46]. This evidence concerns the gene SLC1A2 and central nervous system cancer.