In RA, FLS respond to inflammatory cytokines including interleukin (IL)-1β, 6, 8, 12, 17, 18, 21, tumor necrosis factor (TNF)-α and interferon (IFN)-γ through the activation of multiple intracellular signaling pathways including extracellular signal-regulated protein kinase (ERK), c-Jun amino-terminal kinase (JNK) and p38 mitogen activated protein kinase (MAPK), leading to the expression of multiple cytokines such as IL-1β, IL-6, and TNF-α, as well as the secretion of MMPs that contribute to tissue destruction [3,5-8]. The gene discussed is TNF; the disease is rheumatoid arthritis.