The pathogenesis of RA involves activation of adaptive immunity (CD4 + T cells and autoantibody producing B cells), synovial inflammation with infiltration of immune cells and release of pro-inflammatory cytokines (e.g., TNF-α) culminating in the destruction of cartilage and bone (Schopf et al., 2006; McInnes and Schett, 2011). The gene discussed is TNF; the disease is rheumatoid arthritis.