Downregulation of several key mediators of RA, including TNF-α, IL-1β, IL-6, IL-8, and CCL2, by abatacept may provide an advantage because several downstream pathophysiological processes, such as myeloid cell influx into the synovium, fibroblast activation, cartilage degradation, and osteoclast differentiation, are simultaneously influenced by abatacept. This evidence concerns the gene IL1B and rheumatoid arthritis.