In RA, a remarkable pathogenic effector role of synovial fibroblasts is modulation of osteoclastogenesis, a process dominantly carried out by TNFSF11 and opposed by TNFRSF11B [also referred to as osteoprotegerin (OPG)], which is a decoy receptor for TNFSF11. This evidence concerns the gene TNFSF11 and rheumatoid arthritis.