Cytokines such as interleukin-1-beta (IL-1β), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6) [6,7] have been shown to display potent proinflammatory actions and to contribute to the pathogenesis of RA [8] or experimental arthritis, particularly to cartilage and bone damages [9]. The gene discussed is IL1B; the disease is experimental arthritis.