in vivo:−increased nNOS S-nitrosylation and phosphorylation, decreased CaMKII and MKK4 S-nitrosylation and increased CaMKII phosphorylation in global ischemia model or MCAO in rats−decreased caspase-3 cleavage in MCAO model in rats−increased cell density in CA1 in global ischemia model or MCAO model in rats−reduced maximal NO concentration in bilateral common carotid artery occlusion in rats. The gene discussed is CAMK2G; the disease is ischemia.