To sustain their function and proliferation melanoma cells often shift their metabolism from mitochondrial towards glycolytic ATP production.1 However, various oncogenes and tumor suppressors (e.g. c-myc, Ras and Oct1), as well as hypoxia, stimulate mitochondrial metabolism.2, 3, 4, 5 A key oncogenic event in melanoma is the occurrence of mutations in v-Raf murine sarcoma viral oncogene homolog B (BRAF). The gene discussed is MYC; the disease is melanoma.