Generation of citrullinated autoantigens does not explain a pathogenic role for citrullination in ACPA-negative RA, but PADI polymorphisms may be associated with differences in citrullination patterns that may have an adverse influence on the generation of pro-inflammatory mediators (50), regulation of T-cell responses (47, 48), or NET formation (3, 49) potentially leading to tissue damage. Here, PRTN3 is linked to rheumatoid arthritis.