Possible reasons for this discrepancy are that: we included all of the consecutively treated RA patients, and thus the disease duration of the patients varied, whereas previous observations mostly targeted early-stage RA;17–19 we could not separate ACPA or RF and thus combined them to identify the autoantibodies-positive patients; and we were unable to examine the titers of ACPA or RF. This evidence concerns the gene PRTN3 and rheumatoid arthritis.