Importantly, KRAS and BRAF may contribute to colorectal cancer phenotypes via metabolic reprogramming; for example, the DLD‐1 and RKO colorectal cancer cell lines, which have oncogenic mutations in KRAS and BRAF, display increased expression of the primary glucose transporter SLC2A1 (commonly known as GLUT‐1) and exhibit a Warburg effect phenotype, with the increased glucose consumption rate and concomitant increased lactate production rate in isogenic colorectal cancer cells 62. Here, KRAS is linked to colorectal cancer.