Initially, a “molecular mimicry hypothesis” has been proposed, suggesting that the immune response directed against the bacterial DnaJ protein cross-reacts with the human homologous protein(s) and promotes development of RA; an infection with various bacterial species could trigger the response, since DnaJ is highly conserved among bacteria (Albani et al. 1995; Albani and Carson 1996). The gene discussed is DNAJA2; the disease is infection.