Further evidence for the role of IL-17 in RA is provided by its biological properties in vitro and in vivo, as it induces monocyte- and fibroblast-derived pro-inflammatory cytokines (TNFα, IL-1β, IL-8), mediators of bone and cartilage damage such as matrix metalloproteinases and RANK-ligand (RANKL) [4], [5], [6], neutrophil and monocyte recruitment [7], [8], and osteoclastogenesis [9]. The gene discussed is TNF; the disease is rheumatoid arthritis.