Improved understanding of T-cell biology, with recognition of antigen-independent T-cell influences strongly supports the involvement of T cells in RA pathogenesis.16, 17 The relative inefficacy of T-cell depletion strategies led to the concept of modulating as opposed to depleting T-cell function, with the targeting of one of the more prominent T-cell co-stimulatory signals, the CD28:CD80/CD86, by interaction with abatacept. This evidence concerns the gene CD86 and rheumatoid arthritis.