Several studies have demonstrated the benefits of ACAT1 blockade in AD: ablation of ACAT1 gene in 3XTg-AD mice led to great reduction of Aβ levels and ameliorated cognitive deficits, accompanied by an increase of the beneficial 24-hydroxycholesterol [380]; the P301L tau mouse model lacking ACAT1 exhibited up-regulated autophagosome formation and decreased P301L-tau protein content [381]; in AD patient-derived neurons, ACAT1 inhibition resolves the suppressive effect of CE on tau proteostasis [382]. The gene discussed is MAPT; the disease is Alzheimer disease.