Antioxidant treatment promotes metastatic spread38 and resistance to anoikis31, while subjecting melanoma cells with heightened reliance on catabolism to chronic BRAF-inhibitor treatment allows an alternate epigenetic fate that involves attenuated mitochondrial function with a shift towards reliance on extracellular matrix-dependent processes; however with compromised ability to respond to certain metabolic insults including HMGCR inhibition. The gene discussed is BRAF; the disease is melanoma.