To determine the underlying cause of the abrupt JNK inactivation following cerebral ischemia, phosphorylation of JNK at Thr183/Tyr185 and its upstream molecules Akt at Ser473, SEK1 at Ser80 and MKK-7 at Ser 271/Thr275 were examined in the rat hippocampus following ischemia. This evidence concerns the gene AKT1 and Cerebral ischemia.