Chronic inflammation in COPD could result in local hypoxia in inflamed or remodeled tissues (lungs) via decreased supply (i.e., reduced O2 diffusion through edematous tissue, airway, and thickened mucus or through vascular shunting and decreased O2 delivery to the epithelium), or it could occur via increased demand due to excessive O2 consumption by epithelial cells which ultimately leads to activation of the HIF-1α pathway. The gene discussed is HIF1A; the disease is chronic obstructive pulmonary disease.