In the case of colon cancer, the great majority of tumors are initiated by mutation of the tumor suppressor Adenomatous Polyposis Coli (APC), which is a component of the destruction complex that normally degrades the transcriptional regulator β-catenin, leading to its accumulation in the nucleus and benign polyp formation (Kinzler and Vogelstein, 1996; Segditsas and Tomlinson, 2006). This evidence concerns the gene APC and neoplasm.