Consistent with previous epidemiological studies and in vitro cell experiments, CSE upregulated ACE2 and TMPRSS2 expression, increasing the cells' vulnerability to viral infection.[12, 13, 14, 15, 16, 17] TCGA data analysis demonstrated increased levels of ACE2 and TMPRSS2 in smokers, which decreased after smoking cessation (Figure S1, Supporting Information). Here, ACE2 is linked to viral infectious disease.