CRC develops through a well-established sequence of events that are characterized by specific mutations: inactivating APC mutations lead to the development of a small benign adenoma; activating KRAS mutations are associated with the formation of a large adenoma; and diverse mutations in TP53, PIK3CA, and TGF-β pathway genes drive the evolution of a malignant carcinoma [1, 2]. The gene discussed is KRAS; the disease is colorectal carcinoma.