In this study we investigate lung cells and tissues from COPD patients and cigarette smoke-exposed mice, and an ex vivo model of cigarette smoke extract-treated human alveolar macrophages to explore the hypothesis that the AIM2 inflammasome is activated in the airways of COPD patients and in response to cigarette smoke, and that this activation is associated with a nuclear-to-cytoplasmic shift of distribution of AIM2. The gene discussed is AIM2; the disease is chronic obstructive pulmonary disease.