Over 90% of CRC cases are sporadic, arising from transition from normal mucosa to adenoma, followed by the development of carcinoma usually involving mutations in antiproliferative genes, which include APC (adenomatous polyposis coli), and proliferative tumorigenic genes, such as K-ras and p53. CRC is not solely a hormone-dependent cancer compared to predominantly oestrogen- or androgen-driven cancers such as breast or prostate, respectively. The gene discussed is KRAS; the disease is colorectal carcinoma.