For instance, global ischemia transiently increases Akt phosphorylation and decreases the phosphorylation of the Akt targets, GSK3β and FOXO3A, and activates caspase-3 in the CA1 subfield shortly (1–3 h) after ischemia; acute post-ischemic E2 rapidly inhibits these early events and provides histological protection in young OVX females [42]. The gene discussed is AKT1; the disease is ischemia.