In conclusion, the current study provides evidence of an important role of Rac1 GTPase in ischemia/reperfusion injury-induced NADPH oxidase activation, O2− production and oxidative stress in the hippocampal CA1 region following GCI, and thereby contributes significantly to the delayed neuronal cell death and to a negative functional cognitive outcome following cerebral ischemia. Here, RAC1 is linked to brain ischemia.