Moreover, both heightened NFκB signaling (17) and increased GRM1 expression (18), which foster glutamate-mediated MAPK-driven melanoma cell survival and the AKT–mTOR–HIF1 pathway (19), have been shown to support melanoma-associated proangiogenic signaling, thereby favoring melanoma growth and dissemination. This evidence concerns the gene AKT1 and melanoma.