Infections have been considered as important risk factors associated with the development of rheumatoid arthritis (RA) and mechanisms are related to molecular mimicry as reported for cytomegalovirus (CMV), Epstein-Barr virus (EBV) and parvovirus B19 (1); to citrullinated peptides derived from viruses and bacteria as the conversion of arginine to citrulline increases peptide binding affinity to the RA associated HLA-DRB1 shared epitope (2); and to latent viruses and intracellular bacteria present in fibroblast-like synoviocytes (FLS) and self-reactive memory B cells from RA patients (3). Here, HLA-DRB1 is linked to rheumatoid arthritis.