While the specific contribution of perivasculitis to systemic hypoxia was not investigated, it is tempting to speculate based on the effects of FPS-ZM1 that vasculature dysregulation following increased cell death in CD45– cell populations, including type I and II pneumocytes and/or endothelial cells, may contribute to the rapid decline of K18-hACE2 mice between days 4 and 6 after infection. Here, KRT18 is linked to infection.