Even though less than 2% of CRC is colitis‐associated, sporadic CRC shows similar mutations in genes and signaling pathways, such as the Wnt/β‐catenin pathway, K‐Ras or B‐Raf activation, adenomatous polyposis coli (APC) inactivation, transforming growth factor(TGF)‐β, P53, and the DNA mismatch repair (MMR) proteins.(38, 39, 40, 41) The pathogenesis of both CRC types differs in the histological sequence that is followed during development of neoplasia and the initiation of cancer formation. The gene discussed is KRAS; the disease is colorectal carcinoma.