Although the structure of the anti-citGRP78 IgG was not specifically studied in RA, ACPA-IgG molecules show a 10–20 kDa higher molecular weight compared with non-autoreactive IgG, resulting from Fab-linked N-glycosylation that decreases the binding avidity of ACPA for citrullinated antigens [47]. Here, PRTN3 is linked to rheumatoid arthritis.