FCGR2B and rheumatoid arthritis: Although we cannot clearly explain the role of AHAs in RA, it has been proposed that several biological functions of AHAs, such as B cell suppression due to cross-linking the B cell receptor and FcγRIIb, complement amplification via the capture of dimeric C3b due to immune-complex formation of antigen-binding IgG F(ab’)2 and AHA, and the functional restoration of cleaved IgGs without Fc [7].