Due to the heterogeneic dynamism (metabolic plasticity) between glycolysis and OXPHOS of melanoma, the effective blockade of OXPHOS (e.g. using inhibitors of mTORC1) as well as glycolysis (e.g. MAPK pathway inhibitors) has been shown to resensitise melanomas that are resistant to inhibitors of BRAF and other MAPK pathway components, and thus to be a promising form of treatment.64,75 Previous work has shown that upregulation of aerobic glycolysis in tumour cells is due to the presence of mitochondrial DNA (mtDNA) mutations, which were assumed to impair OXPHOS capacity. This evidence concerns the gene BRAF and melanoma.