Regardless of these issues, targeting GluN2B-PSD95 signaling to neurotoxic pathways offers genuine translational potential because it has been recently shown that stroke-induced damage and neurological deficits can be prevented in nonhuman primates by the administration of TAT-NR2Bc as late as 3 hr after stroke onset (Cook et al., 2012). The gene discussed is DLG4; the disease is stroke disorder.