For example, BRAF mutations, present in nearly 60% of melanomas, enhance glycolytic flux via stabilization of hypoxia-inducible factor 1α (HIF1α) and simultaneous inhibition of mitochondrial respiration through suppression of the microphthalmia-associated transcription factor (MITF)/peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α) pathway [22, 23]. Here, HIF1A is linked to melanoma.