A study investigating signaling through glutamate receptors in human cancers showed that increased activity of hypoxia-inducible factors (HIFs) due to hypoxia or von Hippel–Lindau (VHL) loss-of-function in ccRCC augmented the release of glutamate, which was mediated by HIF-dependent expression of the SLC1A1 and SLC1A3 genes encoding glutamate transporters (11). This evidence concerns the gene SLC1A1 and cancer.