As well, autocrine activation of glioma-derived NMDAR and AMPAR resulted in increased glioma invasion [33] and tumor growth, suggesting that pharmacological targeting of relevant glutamate receptors (NMDAR, AMPAR) or systems that mediate glutamate release (EGF, xCT) may slow disease progression while simultaneously limiting common disease co-morbidities. This evidence concerns the gene SLC7A11 and central nervous system cancer.