Moreover, it has been discovered that post-translational modifications of ACPAs seem to contribute to the pathogenesis of RA, such as the extensive glycosylation of the IgG ACPA V domain, or a decrease in Fc galactosylation and an increase in the Fc fucosylation of serum ACPA IgG1, which predisposes one to RA development [37,44,45]. Here, PRTN3 is linked to rheumatoid arthritis.