Intriguingly, the key melanoma oncogene, B-Raf was shown to suppress oxidative metabolism by inhibiting MITF-induced induction of PGC-1α and melanomas treated with B-Raf inhibitors, such as vemurafenib, were critically dependent on oxidative metabolism for survival suggesting that inhibitors of mitochondrial metabolism may synergize with B-Raf inhibitors in melanoma therapy (119). The gene discussed is BRAF; the disease is melanoma.