Our prospective longitudinal cohort study of the FDR of INA RA patients has afforded us the opportunity to explore the pre-clinical period of individuals who ultimately developed seropositive RA, comparing them to individuals in whom autoantibodies were not detected, and particularly to ACPA seropositive individuals in whom the autoimmune processes did not appear to progress during the observation period (5). The gene discussed is PRTN3; the disease is rheumatoid arthritis.