While the K18-hACE2 murine model has been informative in shedding light on mechanisms of lung injury and dysfunction, it fails to faithfully recapitulate several key histologic features of severe and lethal cases of COVID-19 in humans, such as diffuse alveolar damage (DAD) with hyaline membrane formation and multi-organ failure associated with hypercoagulability and widespread microvascular fibrin thrombi [57]. This evidence concerns the gene KRT18 and COVID-19.