The role of TLR signalling in intestinal tumorigenesis has been studied through the crossing of myeloid differentiation primary response 88 (MyD88)‐deficient mice that have impaired TLR4 signalling, with Apc (ApcMin/+) mice that mimic sporadic cancer and familial adenomatous polyposis. The gene discussed is APC; the disease is Familial adenomatous polyposis.