Taken together, we bring in situ evidence of VWF-rich thrombi in the lungs, draining pulmonary lymph nodes, and heart tissue of patients who died of COVID-19, which we context as likely attributable to COVID-19, supporting the hypothesis that high levels of VWF and dysregulation of the VWF/ADAMTS13 ratio contribute to the incidence of (micro)thrombotic complications influencing COVID-19 morbidity. This evidence concerns the gene VWF and COVID-19.