NFKB1 and COVID-19: Based on these investigations with a model of normal small airway epithelia and other normal lung epithelial cells, we predict that increased TNFα/NFκB- and ENaC- dependent inflammation in the COVID-19 airway is due to inhibition of CFTR signaling by SARS-CoV-2 spike protein, thus inducing a pro-inflammatory clinical phenotype in lung epithelia.