In addition, glycolytic-dependent BRAF-mutant melanoma cells are more sensitive to the BRAF inhibitor vemurafenib, while resistant cells display upregulation of the mitochondrial biogenesis co-activator PGC1α through the melanocyte master regulator microphthalmia-associated transcription factor (MITF), leading to resistance to the original treatment and sensitivity to OXPHOS inhibitors [83]. The gene discussed is BRAF; the disease is melanoma.