Although CEP‐1 has previously been discussed as a candidate autoantigen involved in the etiology of RA, since antibodies to citrullinated P gingivalis α‐enolase cross‐react with antibodies to CEP‐1 and therefore may be involved in breaching tolerance in RA 45, this is the first study to link ACPA reactivities with other periodontal pathogens. This evidence concerns the gene PRTN3 and rheumatoid arthritis.