Dysregulation of cytokines, including tumor necrosis factor (TNF) and interleukin-6 (IL-6) , is involved in joint destruction in rheumatoid arthritis (RA) . TNF and IL-6 induce the differentiation and activation of osteoclasts. They also provide the formation of pannus through the synthesis of vascular endothelial growth factor (VEGF) . In addition, they contribute to the production of matrix metalloproteinases which digest collagen and proteoglycan of cartilage and bone. Biologic agents targeting these cytokines have provided beneficial outcomes, such as achievement of clinical remission, protective effects against joint destruction, and improvement in quality of life (QOL) in RA patients.