SOAT1 and Alzheimer disease: Additionally, the similarities between harmful MAM disruptions observed in AD (i.e., increased ER–mitochondria contact, cholesterol buildup, enhanced calcium transfer and phospholipid synthesis [23,37,100]) and the beneficial response to ACAT1/SOAT1 inhibition (i.e., increased ER–mitochondria contact and cholesterol buildup) are at odds with each other and require further investigation in cells modeling the disease.