Anatomy: Advanced knowledges of cellular and molecular biology led to the development of therapies of rheumatoid arthritis(RA). Rheumatoid arthritis (RA) is a chronic, recurrent, systemic inflammatory disease and results in major deformity or dysfunction of joints. Etiology: Rheumatoid arthritis is now concevied as autoimmune disease. There have been many trials to define the immunological changes in rheumatoid arthritis. But now pathogenesis and significance of immunoglobulin complement and rheumatoid factor are not full accepted. Syndrome: Joints are characteristically involved with early inflammatory changes in the synovial membrane, peripheral portions of the articular cartilage, and lation tissue(pannus) forms, covers, and erodes the articular cartilage, bone and ligaments within the jiont capsule. Inflammatory changes also occur in tendon sheaths(tenosynovitis), and if subjected to a lot of friction, the tendons may fray or rupture. Extra-articular pathological changes sometimes occur, these include rheumatoid nodules, atrophy and fibrosis of muscles, and mild cardiac changes. Treatment: Tumor necrosis factor(TNF) inhibitor for the treatment of rheumatoid arthritis(RA) induces not only significant improvement of symptoms and signs of RA but also substantial inhibition of progressive joint damage.