Deregulation of the Wnt/ß-catenin signaling pathway was shown to be the primary driver of colon cancer development: the vast majority of sporadic human colon cancers harbor loss-of-function (LOF) mutations of the adenomatous polyposis coli gene (Apc) and less frequently gain of function (GOF) mutations of the ß-catenin encoding proto-oncogene Ctnnb1 [11]. The gene discussed is APC; the disease is colonic neoplasm.