KRAS and NRAS, which have been shown to exhibit somatic mutations in 30–40% and 2–5% of human CRCs, respectively,2, 3, 4 are known predictors for resistance to treatment with anti-epidermal growth factor receptor antibodies.5, 6, 7, 8 Although these biomarkers have enabled the development of individualized therapies, especially for the treatment of CRCs with wild-type RAS, specific therapeutic agents against RAS-mutated CRC have not yet been established. The gene discussed is KRAS; the disease is colorectal carcinoma.