For example, a rapid increase of O-GlcNAcylation at both Thr308 and Ser473 of AKT resulted by cerebral ischemia promotes neuronal apoptosis through down-regulating AKT activity, suggesting a negative correlation between AKT phosphorylation and O-GlcNAcylation in ischemic stress response [74]. The gene discussed is AKT1; the disease is brain ischemia.