MYD88 and Familial adenomatous polyposis: Multiple intestinal neoplasia mice with a point mutation in Apc (ApcMin/+) mimic sporadic cancer and familial adenomatous polyposis, and have been used to study the role of TLR signaling in intestinal tumorigenesis through the crossing with MyD88-deficient mice (MYD88-deficient × ApcMin/+).