Therefore, if certain bacterial infections lead to the initiation of an ACPA response, our study and others 9, 10, 20, 21 suggest that infections such as periodontitis, BR, and others yet to be defined induce a low‐titer, low‐avidity, non–citrulline‐specific ACPA response in the early phases of tolerance breakdown, which subsequently evolves into the higher‐avidity, higher‐titer, and highly citrulline‐specific responses that characterize RA. The gene discussed is PRTN3; the disease is rheumatoid arthritis.