Macrophages and neutrophils contribute to the initiation and progression of COPD pathogenesis by increasing chronic inflammation, development of emphysema, and airway epithelium remodeling, which are mediated by increased expression of MMPs, neutrophil elastase, myeloperoxidase, and various pro-inflammatory cytokines and chemokines [14, 37]. The gene discussed is ELANE; the disease is pulmonary emphysema.