Many colorectal cancer cases exhibit the mutation or deletion of tumor protein p53 (TP53) and adenomatous polyposis coli (APC), furthermore, they are supported by gain-of-function mutation in the catenin beta 1 (CTNNB1) gene which leads to the constitutive Wnt signaling activation, a pivotal event in the initiation of adenomas with protruding appearance (polypoid) [30,31]. The gene discussed is APC; the disease is colorectal cancer.