However, autoantibody levels were not significantly reduced [92], suggesting antibody-independent functions of B cells in RA-like antigen-presentation to T cells [93], secretion of proinflammatory cytokines, regulation of the functions of T cells [94], facilitation of lymphoid tissue organization during synovitis [95], and the activation of osteoclasts by secreting receptor activator of nuclear factor kappa-B ligand [96] also contribute to disease development. This evidence concerns the gene TNFSF11 and rheumatoid arthritis.