Since these alterations make them more susceptible to BRAF inhibitors [20], resistant melanomas reprogram their metabolism toward oxidative phosphorylation in response to glycolysis impairment induced by BRAF inhibition [18], increasing their mitochondrial biomass and activity [21,22], as well as enhancing anaplerotic reactions, e.g., the glutamine pathway [23,24]. The gene discussed is BRAF; the disease is melanoma.