Although several studies have demonstrated that cigarette smoke induces various functional changes in macrophages in COPD patients [15], including alterations in glutamine metabolism [16], phagocytic capacity, and levels of inflammatory cytokine secretion [17], the regulatory role of CCL2 on macrophage homeostasis remains obscure, and its pathogenic contributions to COPD have yet to be comprehensively dissected. The gene discussed is CCL2; the disease is chronic obstructive pulmonary disease.