Colorectal cancer (CRC) cells frequently display a constitutively active WNT–β-catenin signaling pathway as a consequence of mutations in APC or other genes that encode the APC-based protein destruction complex or β-catenin itself, which allows β-catenin to accumulate in the nucleus and contribute to cellular transformation (Barker and Clevers, 2006, Krausova and Korinek, 2014). The gene discussed is APC; the disease is colorectal carcinoma.