In a recent study, Odqvist et al. demonstrated that a mutation in the A20 DUB domain causes upregulation of PADI4, leading to increased protein citrullination and extracellular trap formation, suggesting that citrullination and NETs act as upstream pathogenic mechanisms driving RA and SLE autoimmune pathology in patients with A20 mutations12. The gene discussed is TNFAIP3; the disease is systemic lupus erythematosus.