The nature of the coagulopathy seen in COVID-19 has been repeatedly characterised by elevated D-dimers and fibrin degradation products (FDP), mild thrombocytopaenia, and prolonged prothrombin time with pulmonary coagulation and fibrinolysis purported to be influenced by, and correlate to, certain proinflammatory cytokines [2, 6–8]. The gene discussed is F2; the disease is COVID-19.