Soga et al. demonstrated that (1) CRC metabolism changes from the benign tumor stage but does not depend on the stage; (2) the Myc protein, an oncogene product, alters the metabolism of CRC through 215 metabolic reactions; (3) suppression of Myc and metabolic enzymes controlled by Myc inhibits the growth of CRC cells; and (4) Myc-controlled pyrimidine metabolic pathways are promising targets for CRC treatment [29]. The gene discussed is MYC; the disease is benign neoplasm.