Interestingly, increases of both tissue plasminogen activator and PAI-1 in all COVID-19 patients regardless of disease severity suggest that severe SARS-Cov2 infection may hijack normal profibrinolytic signaling and lead to a procoagulant state, including increased PAI-1 expression, prolonged PAI-1 half-life, and severe lung injury (185, 186). Here, SERPINE1 is linked to COVID-19.