Moreover, ABT may be induced to improve synovial inflammation through terminating inflammatory cytokine networks by, in part, inhibiting ADAM17 and consequently disease activity in RA patients as well as the inhibition of T lymphocyte activation, although direct mechanisms or interaction of inflammatory mediators such as TNFα, IL-6 and CX3CL1 by ABT therapy have not been still resolved in the present study. The gene discussed is CX3CL1; the disease is rheumatoid arthritis.