Although the specific mechanisms for the preservation of mitochondrial structure and function conferred by PVN-OXT neuron activation after an MI remain to be rigorously tested, activation of Akt and AMPK (Fig. 2C) are likely candidates because these kinases have been implicated in the prevention of mitochondrial dysfunction by electronic VNS after ischemia/reperfusion injury [6, 86, 106, 125]. The gene discussed is AKT1; the disease is ischemia.