By extension, decreased disease risk is likely associated with decreased IL-6 trans-signaling (which requires sIL-6R and is mainly pro-inflammatory) but increased IL-6 classic signaling (which requires mIL-6R and is thought to be mainly regenerative and protective).98 On the basis of these genetic findings, it was not immediately obvious what to expect from a drug such as TCZ (approved therapeutic for rheumatoid arthritis and other auto-immune diseases), which blocks both sIL-6R and mIL-6R. The gene discussed is IL6; the disease is rheumatoid arthritis.