Hyperproliferative synovial fibroblasts play a critical role in the pathogenesis of RA by the following mechanisms: They directly invade bone and cartilage, produce proinflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin (IL)-1β [1], destroy cartilage through the production of metalloproteinase [2], and produce the receptor of nuclear factor-kappa B (NF-κB) ligand, which augments osteoclast activity for bone destruction [3-5]. The gene discussed is IL1B; the disease is rheumatoid arthritis.