Our data suggest that the inhibition of excessive oxidative stress by N-acetylcysteine (NAC), an antioxidant which has been proven by us [28, 29] and others [30] to attenuate myocardial I/R injury in diabetes, could restore Cav-3 expression, which subsequently improves PI3K/Akt and JAK2/STAT3 signaling and ultimately restores RPC cardioprotection in diabetic rats. This evidence concerns the gene AKT1 and diabetes mellitus.