The glycolytic pathway of melanoma cells intrinsically relies on the activation of signaling pathways, such as (i) the MAPK pathway that, hyperactivated in BRAFV600E-driven melanomas, controls HIF-1α and MYC activities (42, 43) and (ii) the PI3K/AKT/mTOR pathway which is hyperactivated upon loss of PTEN [another common alteration found in melanoma patients (44)] or upon AKT and PI3K activating mutations (45, 46). This evidence concerns the gene AKT1 and melanoma.