Conversely, we can hypothesize a different pathogenesis for hypercoagulable state and higher risk of thrombotic events in older COVID-19 patients, in whom an impaired endogenous fibrinolysis may be prevalent; this is in line with previous evidence demonstrating an age-dependent increase of molecules antagonizing thrombus lysis (i.e. plasminogen activator inhibitor) [23]. Here, SERPINB2 is linked to COVID-19.