The progression of CRC frequently involves the increased activity of Kirsten rat sarcoma virus (KRAS) or/and beta-catenin pro-oncogenes, along with the loss of functions of tumor suppressors, including Adenomatous polyposis coli (APC), SMAD4, and p53, with mutation percentages ranging from 10% to 80% (Armaghany et al., 2012; Cancer Genome Atlas, 2012). The gene discussed is APC; the disease is colorectal carcinoma.