The treatment of mice with a soluble IL1RL1-Ig Fc fusion protein as decoy receptor or with a blocking anti-IL1RL1 antibody resulted in a reduction of the collagen induced arthritis [21] and of the inflammatory response in the lung [25] proving the therapeutic potential of the IL-33 and IL1RL1 interaction. The gene discussed is IL1RL1; the disease is arthritic joint disease.