The lower target affinity induced by N-glycosylation of the RA ACPA-IgGs suggests a lower pathogenicity for these antibodies; however, the Fc-linked aberrant decrease in galactosylation and increase in fucosylation patterns observed in RA patients further increases a more pro-inflammatory phenotype of these antibodies [48,49]. This evidence concerns the gene PRTN3 and rheumatoid arthritis.