We read with much interest the recent observational study of Nougier et al., which aimed at studying thrombin generation (TG) and fibrinolysis profiles of COVID‐19 patients admitted to an intensive care unit (ICU) or to an internal medicine ward and receiving various schemes of prophylactic heparin.[1] They reported that thrombin potential remained within normal range despite heparin and that fibrinolysis was decreased in relation with increased plasminogen activator inhibitor 1 (PAI‐1) and thrombin‐activatable fibrinolysis inhibitor (TAFI) antigen plasma levels. Using the rotational thromboelastometry (ROTEM) delta device with EXTEM reagents and the addition of 0.625µg/mL tPA (referred to as ‘TEM‐tPA'), they reported decreased clot lysis in COVID‐19 patients, which was more pronounced in patients who presented a thrombotic event, compared to event‐free patients.