In a recent study, Odqvist et al. proposed a mechanism suggesting that increased PAD4-dependent protein citrullination and neutrophil extracellular trap (NET) formation contribute to the development of anti-cyclic citrullinated peptide (anti-CCP) antibodies and autoimmune pathology in RA and SLE patients with A20 DUB-domain mutations12. The gene discussed is PADI4; the disease is rheumatoid arthritis.