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. This evidence concerns the gene PADI4 and rheumatoid arthritis.