Neutrophils are used by the innate immune system to form thrombi during many types of thrombosis. The inactivation of endogenous anticoagulants results in increased intravascular coagulation by increasing factor XII activation, decreasing plasmin production, or boosting the tissue factor-dependent extrinsic pathway. The creation of neutrophil extracellular traps (NET) by the externalization of decondensed nucleosomes and granule proteins supports neutrophil-dependent prothrombotic processes. Experimental thrombosis has been demonstrated to be caused by these traps, whether intact or fragmented, since they provide the means to enhance microvascular thrombosis. The von Willebrand factor increases platelet adhesion when neutrophils and activated platelets combine to form NET. Thus, neutrophils and externalized nucleosomes promote intravascular blood coagulation and thrombosis during infections and during conditions resulting from blood vessel damage.