Rather, we suggest that release of PAD from neutrophils in the joints of RA patients represents a later event in the disease process, during which citrullinated proteins and preexisting ACPAs form proinflammatory immune complexes and drive a continuous inflammatory response in the joints, which may be supported by our finding of significantly higher DNA levels in ACPA‐positive RA patients compared to ACPA‐negative RA patients. This evidence concerns the gene PADI4 and rheumatoid arthritis.