Interestingly, cultured colorectal cancer cells (CRC) harboring KRAS or BRAF mutations, which upregulate the glucose transporter Glut1, are selectively killed when exposed to high levels of vitamin C, but this is not due to the antioxidant function of vitamin C. Instead, this effect is mediated by the increased uptake of the oxidized form of vitamin C, dehydroascorbate (DHA) via the Glut1 glucose transporter, which is subsequently reduced to vitamin C, thereby depleting glutathione and causing oxidative stress. This evidence concerns the gene KRAS and colorectal carcinoma.