Taken together, our results suggest that the formation of a proinflammatory microenvironment might be the main culprit, resulting in a vicious cycle in which many CD4+CD25−Foxp3+ T cells induced by cigarette smoke or other factors in turn facilitated the differentiation and proliferation of naïve CD4+ T cells into Th17 cells, which eventually contributes to the amplification and perpetuation of chronic inflammation in COPD. The gene discussed is CD4; the disease is chronic obstructive pulmonary disease.