The Wnt/β-catenin signaling pathway is abnormally activated in cancer cells, which has mainly been attributed to somatic mutations in the Wnt signaling component, adenomatous polyposis coli (APC), as well as β-catenin gene mutations that occur in approximately 90% of CRC patients, that disrupt the Wnt gradient and cause ISCs to proliferate along the crypt–villus axis [16,17,18]. This evidence concerns the gene APC and colorectal carcinoma.