Given the role of AR and GR activation in acute air pollution-induced lung injury and inflammation6–8,14, and the use of AR and GR agonists in treatment of chronic asthma and COPD, it is conceivable that patients receiving bronchodilators and/or immunosuppressants might have differential inflammatory processes induced after acute air pollutant exposures15–18. The gene discussed is AR; the disease is chronic obstructive pulmonary disease.