Abatacept has been extensively used to treat RA by interfering with T-cell immune activity. It functions as a fusion protein composed of the Fc region of IgG1 fused to the extracellular domain of CTLA-4 [4]. Its binding to CD80 and CD86 molecules on antigen-presenting cells inhibits T-cell activation [4,8]. Although preventing T-cell activation by interfering with signaling via CD28 still represents its main mechanism of action, abatacept also acts on additional immune cell populations such as regulatory T cells, monocytes/macrophages, osteoclasts, and B cells [8]. This evidence concerns the gene CD86 and rheumatoid arthritis.