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An active pool of __Tissue Factor__ (TF) is required to initiate blood coagulation, but the mechanism that regulates the activation of TF is highly debated. The reduced coagulant activities of both human and mouse disulfide-mutated TF indicates that the formation of a Cys186-Cys209 or Cys190-Cys213 disulfide bond in the extracellular domain of TF controls its procoagulant function. Also the strong evolutionary conservation of this allosteric disulfide bond supports previous assumption. Procoagulant active TF is also found intravascularly on small vesicles (microparticles), and high levels of microparticle-associated TF is thought to increase the risk for thrombosis in cancer patients. Despite the fact that chemotherapy is an independent risk factor for thrombosis, chemotherapy-induced tumor destruction was not associated with an increase in microparticle-associated TF in testis cancer patients. The soluble isoform of TF, alternatively spliced TF (asTF), induces angiogenesis through interaction with integrins and independent of intracellular protease-activated receptor (PAR)-mediated signaling. PAR-2 but not PAR-1 plays a role in arteriogenesis in vivo. Furthermore, PAR-2 is involved in the anti-inflammatory response that may promote arteriogenesis.