A recent comparison between prophylactic and therapeutic IVIg treatments in several murine disease models (ITP, arthritis and skin-blistering disease) has shown that the anti-inflammatory effects of IVIg were similar, and were dependent on FcγRIIB expression and sialylation, although SIGN-R1 was not essential in all disease models when IVIg was administered therapeutically (14). The gene discussed is FCGR2B; the disease is arthritic joint disease.