Specifically, the alternative pathway (AP) and C5aR of complement is required for the perpetuation and severity of disease, as mice lacking complement MASP-1/3, factor D, factor B, C5, and C5aR are substantially resistant to arthritis while mice lacking C1q, C4, mannose-binding lectin, FCN A, Collectin 11, and FCN A are susceptible to arthritis (5, 8–12). The gene discussed is COLEC11; the disease is arthritic joint disease.