Although we observed an increase of G0 IgG4 glycans in patients with IgG4RD, and the proinflammatory nature of G0 glycans has been reported in a number of inflammatory diseases, it is not clear whether agalactosylated IgG4 is involved in the pathogenesis of IgG4RD because IgG4 has a low binding ability to FcγR. This evidence concerns the gene FCGR2A and immunoglobulin G4-related sclerosing disease.