For example, activating mutations in BRAF or NRAS proteins hyperactivate the RAS/RAF/MEK/ERK MAP kinase (MAPK) pathway in melanoma cells, which increases glucose consumption and aerobic glycolysis [4]; and treatment with inhibitors targeting mutant-BRAF (BRAFi) or MEK (MEKi) inhibits glycolysis, forcing many melanomas to alter their metabolism towards increased mitochondrial oxidative phosphorylation (OxPhos) and utilize alternate fuels like fatty acids or glutamine [5–7]. The gene discussed is BRAF; the disease is melanoma.