These observations are of possible significance in relation to the role of smoking and HLA genotype in the immunopathogenesis of RA, seemingly strengthening the link with smoking-related protein citrullination in the airway mucosa17–19, and possibly the gastrointestinal mucosa20,21, resulting in interactions of citrullinated proteins with SE-expressing T lymphocytes, leading to the production of potentially pathogenic ACPA-IgA auto-antibodies13. Here, PRTN3 is linked to rheumatoid arthritis.