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. The gene discussed is PRTN3; the disease is rheumatoid arthritis.