Importantly, treatment of vemurafenib-resistant BRAFV600E melanoma cells with vemurafenib in combination with the pyruvate mimetic dichloroacetate, which inhibits glycolysis as a consequence of an increase in glycolysis-derived pyruvate flux into the TCA cycle [112], was shown to restore the expression of glycolytic enzymes and re-sensitize these resistant cells to vemurafenib [98], indicating that glycolysis contributes to resistance to BRAF/MEK/ERK pathway inhibition in melanoma. This evidence concerns the gene BRAF and melanoma.