Homologous to human Apc, deregulation of Wnt/β-catenin signaling following inactivating mutation in the wild-type allele of this gene is the major initiating factor in the etiology and pathogenesis of familial adenomatous polyposis (FAP) and frequently found in more than 80% of sporadic CRC in human patients [30, 32]. This evidence concerns the gene APC and Familial adenomatous polyposis.