In the early 1990s Fearon and Vogelstein 2 postulated that mutations in CRC occur in a sequential manner, with specific mutations being associated with tumour initiation, eg the adenomatous polyposis coli (APC) gene, and other mutations occurring later that drive progression, eg TP53. Recent DNA sequencing studies confirmed the common co‐existence of these mutations within individual CRC tumours. Here, TP53 is linked to colorectal carcinoma.