It was predicted that NO-DMA would retain the neuroprotective actions of DMA, since previously we have shown that the neuroprotective actions of raloxifene and DMA are GPR30-dependent and mediated via PI3K/Akt signaling in primary neuronal culture in the oxygen glucose deprivation (OGD) assay, a composite model of ischemia-reperfusion injury [47]. The gene discussed is AKT1; the disease is ischemia.