evidence: Lung tissues from patients with fatal COVID-19 have revealed pathology cascades that include progressive diffuse alveolar damage, alveolar–capillary barrier damage, surfactant-production loss, and increased vascular permeability. Such findings typify those of severe acute respiratory distress syndrome. However, based on the detection of viral protein and RNA remnants, the same lung tissues also reveal novel pathology cascades that are distinct from those of pandemic influenza and SARS-CoV infection, and that arise from direct SARS-CoV-2 infection of respiratory epithelial and basal cells, alveolar type 1 and 2 cells, and capillary endothelial cells. Infection triggers pathways involved in the senescence pf epithelial and endothelial cells, impaired epithelial repair, increased procoagulants (e.g., PAI-1 or SERPINE1) in endothelial cells and neutrophils, coagulopathies from inhibition of fibrinolysis, and pulmonary fibrosis (Fig. 1b). The associated alveolitis and endotheliopathy culminates in dead lung acinar units that cannot replenish cells and thereby recover1. [...] Are COVID-19 coagulopathies due to pre-existing systemic endotheliopathies or a cause of them? [...] Using autopsies to dissect COVID-19 pathogenesis