Additionally, the use of PlauGFDhu/GFDhu mice in which a 4 aa substitution into the growth factor domain of uPA precludes its binding to uPAR while preserving other functions of the protease and its receptor [36] indicated that binding of endogenous uPA to uPAR in the perinecrotic area promotes the recovery of dendritic spines following an ischemic stroke. This evidence concerns the gene PLAUR and ischemic stroke.