Compared to the chemically induced and inflammation-associated AOM/DSS model, which is characterized by activating mutations in epithelial pathways such as p53 and K-Ras [26, 28], the ApcMin/+ mouse model relies on deregulation of the Wnt/β-catenin signaling cascade in the first place, therefore addressing another route of intestinal carcinogenesis development. The gene discussed is KRAS; the disease is infectious otitis media.