Overexpression of the Wnt pathway by either inactivation of the adenomatous polyposis coli (APC) gene or activating mutations in β‐catenin (CTNNB1) has been observed in most of the colorectal cancers (CRCs) following the classical adenoma–carcinoma sequence (Vermeulen & Snippert, 2014). The gene discussed is APC; the disease is carcinoma.