However, our study goes further and suggests that the increased susceptibility of COPD epithelial cells to virus infection may also be due to an imbalance between virus-entry-enhancing serine proteases (e.g., TMPRSS4 and CTSB) and inhibitory antiproteases, such as SERPINE1, which is consistent with our previous results that cigarette smoke in COPD chips upregulates the expression of host proteases TMPRSS11E and TMPRSS11F [28]. The gene discussed is TMPRSS11E; the disease is viral infectious disease.