APC and intestinal neoplasm: The well-established model for intestinal tumorigenesis, the C57BL/6J-ApcMin/+ mouse, is heterozygous for the germline nonsense mutation multiple intestinal neoplasia (Min) in the tumor suppressor gene adenomatous polyposis coli (Apc) leading to a truncated nonfunctional APC protein, and therefore develops numerous spontaneous intestinal tumors [3, 4]. Apc is a key component in the Wingless-related integration site (Wnt) signaling pathway [5, 6].