In particular, TNF-α and IL-17 are considered vital to RA pathogenesis, as these proinflammatory factors trigger the release of degradative enzymes that proactively destroy cartilage matrix such as cathepsin K, MMP-1 and MMP-9, as well as additional downstream proinflammatory factors such as PGE2. The gene discussed is TNF; the disease is rheumatoid arthritis.