These findings suggest that (a) there is a transient increase of AKT activity after preconditioning, at the early stage of ischemia (1–2 hr), and after several hrs of reperfusion; (b) increase of AKT activity may have protective effects during ischemia and reperfusion periods; and (c) preconditioning-induced AKT phosphorylation may be not related to the protective effect in lethal ischemia, that occurs several days later. This evidence concerns the gene AKT1 and ischemia.