Blood coagulation is triggered by vessel injury and TF exposure. This triggers extrinsic pathway activation, leading to thrombin generation via the shared pathway and fibrin generation. Alternatively, contact pathway activation via FXII activation by polyP also leads to intrinsic pathway activation, thrombin generation and fibrin deposition in the absence of vessel damage, leading to pathological thrombus formation. Clot growth and size is regulated at multiple stages by endogenous anticoagulants, including tissue pathway inhibitor, the PC pathway and antithrombin. Once the vessel repair is underway, proteolytic clot lysis is orchestrated by plasmin, which breaks down cross-linked fibrin into fibrin degradation products.