A series of molecular alterations in epithelial cells, including mutations of the Wnt signaling suppressor adenomatosis polyposis coli (APC), the tumor suppressor gene p53, and the k-ras oncogene, drive the development of dysplasia or colorectal cancer from colitis in individuals with IBD (Itzkowitz and Harpaz, 2004; Aust et al., 2002; Brentnall et al., 1994; Burmer et al., 1992; Khor et al., 2011; Neurath, 2014). This evidence concerns the gene APC and dysplasia.