Moreover, advances in the understanding of disease mechanisms and novel molecular technologies have contributed to the development of new specific modalities for RA treatment, such as targeting of disease-relevant proinflammatory cytokines (e.g., antitumor necrosis factor-α (TNF-α) or anti-interleukin-6 (IL-6)), blocking the binding of antigen-presenting cells (APCs) to T-cell costimulating channels (cytotoxic T-lymphocyte-associated protein 4-immunoglobulin (CTLA4-Ig)), or the use of B-cell depleting agents (anti-CD20 antibody). This evidence concerns the gene CTLA4 and rheumatoid arthritis.