In light of GLUT1 as a major receptor for uptake of Vitamin C, an interesting study discovered that cultured human colorectal cancer cells with BRAF or KRAS mutations are selectively exterminated after high dose of vitamin C treatment, as a result of elevated GLUT1-facilitated uptake of the oxidized form of vitamin C, namely dehydroascorbate, which indicates a potentially novel therapy for KRAS or BRAF mutant colorectal cancers [43]. The gene discussed is BRAF; the disease is colorectal cancer.