Although the cytosolic activation of Akt by SC79 was sufficient to recapitulate the primary cellular function of Akt signaling, which protected ischemic-injury-induced neuronal death in a hippocampal neuronal culture system and a mouse model for ischemic stroke [29], this was a short-term application in vivo in an ischemic stroke model. This evidence concerns the gene AKT1 and ischemic stroke.