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]. This evidence concerns the gene F3 and acute respiratory distress syndrome.