F12 and COVID-19: Compared to other seasonal CoVs and influenza, we observed marked dysregulation of a genomic signature of VTE28 (‘thrombosis’, Figs. 3A and s1–, s3) and increased expression of many thrombotic pathway genes in a subset of early COVID-19 cases including prekallikrein (KLKB1), Factor 12 (F12), the plasminogen activator inhibitor (SERPINE1) and others, along with decreased expression of antithrombotic protein S (PROS).