Our data implied that chronic cigarette smoke exposure may be associated with high levels of CCR1 found in AMs of patients with COPD, and excessive CCR1 activation in patients with COPD could provoke a dramatic increase in cytokine secretion via JAK/STAT/NF-κB signaling, which is not only effective in facilitating viral clearance but may also further contribute to the exaggerated inflammatory response. This evidence concerns the gene SOAT1 and chronic obstructive pulmonary disease.