Taken together, the present observations of reduced behavioral outcome and axonal remodeling in Plg deficient mice demonstrate that the endogenous Plg-dependent proteolysis is an important element involved in neurological recovery after stroke, suggesting that, in addition to being used as a thrombolytic agent in the circulation system, tPA/plasmin in the CNS parenchyma is neurorestorative, and provides therapeutic benefit by enhancing neuronal remodeling during the convalescence after stroke. This evidence concerns the gene PLG and stroke disorder.