Chronic obstructive pulmonary disease (COPD) is characterized by irreversible airflow limitation in the lungs. Smoking is one of the amongst major risk factors for the development of COPD. Environmental pollution, age, and airway hyperreactivity are also the risk factors. The protease-antiprotease imbalance and the oxidant-antioxidant imbalance cause airway inflammation and destruction. The genes related to these balances may contribute to development of COPD pathology. Candidate gene-association studies and linkage analyses have been reported for COPD patients. The alpha-1 antitrypsin, glutathione S-transferase, microsomal epoxide hydrolase, and matrix metalloproteinase, are candidate genes. In acquired factors for COPD pathology, the adenoviral latent infection may enhance airway inflammation, leading to airflow obstruction. The current progress and future visions of genetic predisposition of COPD are discussed.