In general, severe pulmonary inflammation (acute respiratory distress syndrome (ARDS)) is associated with a significant thrombotic risk, the main mechanisms of which include (i) local expression of tissue factor (TF) on mononuclear cells, its accumulation and release following endothelial damage, which subsequently initiates coagulation initiation and thrombin generation, (ii) as well as inhibition of fibrinolysis in response to the cytokine storm (TNFα, IL-1, IL-6) [24–26]. Here, IL6 is linked to acute respiratory distress syndrome.