Consistent with the in vivo findings, multiple groups demonstrated aberrantly increased ER-mitochondria contacts and/or enhanced MAM function in various cell models of AD which enables more detailed mechanistic studies: for example, overexpression of APP mutants or exposure to nanomolar concentrations of Aβ increases ER-mitochondria contact points and mitochondrial calcium concentrations [193, 195]. The gene discussed is APP; the disease is Alzheimer disease.