Rheumatoid arthritis (RA) is characterised by breach of self-tolerance towards citrullinated proteins (anti-citrullinated peptide/proteins antibodies (ACPA)), which can occur years prior to clinical onset of RA at extra-articular sites.1–6 Several post-translationally deiminated proteins have been indicated as a potential source of citrullinated antigens in the RA joints,3 but to date their cellular source and specific contribution to the lesional ACPA response is unknown. This evidence concerns the gene PRTN3 and rheumatoid arthritis.