Cumulative data indicate that the B-cell response producing ACPA matures, as supported by rising autoantibody levels, isotype switching and epitope spreading.2 However, interestingly, we, and recently Yamada et al,3 showed that the avidity of ACPA is low compared with recall antigens in the same patients.4 While Yamada et al compared the ACPA avidity to other autoantibody responses and showed that ACPA really stands out with its low avidity compared with other autoantibodies in RA, we wondered whether the ACPA response would be different from other anti-PTM responses. Here, PRTN3 is linked to rheumatoid arthritis.