The pathological events in APP/PS1/SREBP2 mice precipitating AD-like symptoms were dependent on mGSH depletion (Figure 4), since in vivo replenishment of mGSH with cell-permeable GSH monoethyl ester (GSHee) attenuated neuropathological features of AD in APP/PS1/SREBP-2 mice, including decreased neuroinflammation, cell death and tau-phosphorylation, which led to improvement of cognitive defects (Barbero-Camps et al., 2013). The gene discussed is APP; the disease is Alzheimer disease.