In support of PRR-signalling importance for both sensing noxae and to initiate barrier repair, mice deficient in myeloid differentiation primary response 88 (Myd88), which encodes a key downstream adaptor protein of all TLR [except TLR3 that signals exclusively via TIR-domain-containing adapter-inducing interferon-β (TRIF/TICAM-1)], are susceptible to experimental colitis induced by dextran sodium sulfate (DSS), a chemical that damages the colonic epithelium30. The gene discussed is MYD88; the disease is colitis.