Apart from a small subset of melanomas, BRAF mutations are associated with increased glycolysis and attenuated oxidative phosphorylation, and such balance is reversed upon treatment with BRAFi.16, 17, 18, 19, 20 Resistance to BRAFi seems to be accompanied by precise metabolic changes as well: higher reliance on oxidative phosphorylation,21, 22, 23, 24 glutamine dependency21, 25, 26 and up‐regulated serine metabolism.26, 27. Here, BRAF is linked to melanoma.