The overactivation of the BRAF/MEK/ERK signaling pathway due to the occurrence of BRAF mutations can also contribute to the regulation of melanoma cell metabolism, as it was demonstrated that BRAFV600E inhibited the MITF-peroxisome proliferator-activated receptor γ coactivator 1α (PGC1α) axis, resulting in enhanced glycolysis and the repression of oxidative metabolism [[72], [73], [74]]. The gene discussed is BRAF; the disease is melanoma.