In a nonhuman primate model of lethal systemic inflammatory response syndrome (SIRS) associated with sepsis, the authors were able to detect FXIa–PAI-1 complexes in the circulation after a bacterial challenge.79In preliminary studies, it was found that inactivation of FXIa by PAI-1 on the EC surface may invoke a signaling pathway to increase vascular permeability by way of cleavage of EC VE-cadherin. The gene discussed is CDH5; the disease is systemic inflammatory response syndrome.