Using a mouse model and melanoma cell lines generated from mouse tumors treated with vemurafenib (BRAF inhibitor) or not, it has been shown that the acquisition of drug resistance is associated with an increase in mitochondrial OXPHOS, growth dependency on the glutamine supply and a compensated increase in glutathione levels, which is associated with strong activation of the nuclear factor erythroid 2-related factor-2 (NRF2) pathway and increased xCT expression [105]. Here, BRAF is linked to melanoma.