Major limitations in the utilization of both wild-type and K18-hACE2 mice have been identified (here and elsewhere) and mainly include marginal disease phenotypes (in wild-type mice) and absence of interstitial pneumonia uniquely depicting the features of diffuse alveolar damage (DAD) and subsequent reparative fibrosis that characterize pneumonia in human patients (absent in both wild-type and transgenic mice). Here, KRT18 is linked to pneumonia.