Consistent with its role in tissue damage and fibrosis, increased expression of IL-33 and ST2L have been observed in chronic non-allergic airway diseases, such as COPD and IPF.7,8 COPD and IPF are debilitating disorders of the lung characterized by chronic airway inflammation and fibrosis that compromise tissue architecture, lung function, and gas exchange. The gene discussed is IL1RL1; the disease is idiopathic pulmonary fibrosis.