Liu A, Zhang X, Li R, et al. - Researchers here examined angiotensin‐converting enzyme 2 (ACE2) location and expression, and its association with gender, age and cigarette smoke (CS), in a CS‐exposed mouse model and 224 non‐malignant lung tissues (125 non‐smokers, 81 current smokers and 18 ex‐smokers) by immunohistochemistry. In addition, they examined the relationships of ACE2 with CS‐induced oxidative stress‐related markers, hypoxia inducible factor‐1α (HIF‐1α), inducible nitric oxide synthase (iNOS), and 4‐hydroxynonenal (4‐HNE). Overexpression of ACE2 was noted predominantly on the apical surface of bronchial epithelium, while there was it was reduced in alveolar epithelium, due to the dramatically reduced abundance of alveolar type II pneumocytes in CS‐exposed mouse lungs. In line with this, human bronchial and alveolar epithelial cells in smokers primarily exhibited significant overexpression of ACE2 regardless of age or gender. Bronchial epithelial cells from ex‐smokers compared with current‐smokers had decreased ACE2 expression, this was especially noted in those who had ceased smoking for more than 10 years. In addition, a positive correlation was noted of ACE2 expression with the levels of HIF‐1α, iNOS, and 4‐HNE in both mouse and human bronchioles. Overall findings suggest that smoking‐induced ACE2 overexpression in the apical surface of bronchial epithelial cells imparts a route by which SARS‐CoV‐2 enters host cells, which supports clinical relevance in reducing the potential transmission risk of COVID‐19 in smoking populations by smoking cessation.