Consistent with our findings in the AIA model, the fact that 35–40% of FcγRI,II,III−/− mice developed CIA, whereas γ-chain−/−/FcγRIIb−/−mice that also lack functional FcγRIV were protected from disease development, further supports the role of FcγRIV in this arthritis model [44]. The gene discussed is FCGR2B; the disease is arthritic joint disease.