Deficiency of antiplasmin resulted in the resolution of venous thrombus96 and this prompted efforts to therapeutically target antiplasmin in order to increase endogenous fibrinolytic activity.97 This approach was successful in a model of pulmonary embolism97 and ischemic stroke.98 Indeed, antibodies specific to antiplasmin removed pulmonary emboli in a manner similar to exogenous tPA.97 This evidence concerns the gene PLAT and ischemic stroke.