Inflammatory signaling such as tumor necrosis factor α (TNFα) and interleukin 23 (IL-23) or altered expression of growth factors such as bone morphogenic proteins (BMPs) and Wnts may disturb or misdirect these processes depending anatomical site and/or external stimuli such as mechanical changes as seen in various arthritic diseases including RA and SpA [1, 7]. The gene discussed is IL37; the disease is rheumatoid arthritis.