We and others have shown that antibodies against citrullinated proteins/peptides (ACPA), analysed as anti-cyclic citrullinated proteins (CCP2) antibodies, precede the development of RA by several years [1,2] and that individuals who had the combination of anti-CCP antibodies together with either the human leukocyte antigen-shared epitope (HLA-SE) alleles or with the protein tyrosine phosphatase non receptor type 22 (PTPN22) 1858T variant had a high relative risk of developing RA [3,4]. This evidence concerns the gene PRTN3 and rheumatoid arthritis.