Large-scale GWASs of RA and JIA, respectively, render us prospects to identify potential common mechanisms in disease pathogenesis, which may lead to the identification of potential novel targets for therapeutic intervention and extending treatment strategies from commonly used molecular therapy with antibodies against TNF-α or IL-1 inhibitors to include recent advances in efforts to unravel effective targets influencing autoinflammatory and/or autoimmune processes. This evidence concerns the gene TNF and rheumatoid arthritis.