Susceptibility to RA is associated with HLA-DRB1 locus (shared epitope) and antibodies against citrullinated peptide (ACPA) (3–5), revealing a strict pathogenic relationship between HLA class II-dependent immune response (4, 6, 7) and the determinant role of T cells along with B cells in this disease (8). This evidence concerns the gene PRTN3 and rheumatoid arthritis.