Fibroblasts function as a major source of airway fibrosis and extracellular‐matrix protein deposition, which lead to peripheral airway narrowing in COPD.17, 18 We showed that TUG1 expression was higher in CSE‐treated lung fibroblasts and lower in CSE/shTUG1‐treated lung fibroblasts (Figure 3A). This evidence concerns the gene TUG1 and chronic obstructive pulmonary disease.