Compared to healthy controls, CD14++ CD16− monocytes of RA patients displayed an enlarged capacity to produce proinflammatory cytokines after stimulation with synthetic TLR2 and TLR9 agonists while both CD14++ CD16− and CD14+ CD16+ monocytes showed increased response to EBV stimulation. The gene discussed is TLR9; the disease is rheumatoid arthritis.