We thank Dr. Asada and colleagues for their comments on our article in CHEST (December 2004),1 and we appreciate the opportunity to respond. COPD is characterized by chronic inflammation in the airway and the parenchyma. Inflammatory cells such as macrophages, neutrophils, and CD8+ T lymphocytes release a variety of mediators, proteases, and oxidants. These inflammatory events induce mucus hypersecretion, bronchial smooth muscle hypertrophy, airway hyperresponsiveness, remodeling and narrowing of the small airways, and parenchymal destruction, all of which result in airflow limitation. Based on this pathogenesis, we conducted a case-control association analysis for some polymorphisms of the interleukin (IL)4, IL13, and ADRB2 genes. Similarly, IL1β is a good candidate gene for COPD association analysis.