The findings that experimentally infected mice deficient in CD14 [25],[27], TLR2 [14],[28] developed even more severe arthritis than their wild type counterparts, and that mice lacking the TLR adapter protein myeloid differentiation factor 88 (MYD88) [29] also developed arthritis, provided the first clear indication that intact spirochetes may employ additional TLRs and/or TLR-independent pathways to induce acute inflammation. The gene discussed is TLR2; the disease is arthritic joint disease.