Our findings in human iPSC-derived AD neurons indicate that alterations in neuronal CE could drive pTau accumulation and are supported by previous in vivo observations in mouse models showing that statins reduce NFT load in animal models of tauopathy (Boimel et al., 2009), and genetic inhibition of cholesterol esterification by ACAT1 reduces tauopathy in an AD-mouse model (Shibuya et al., 2015), indicating that the interactions between CE and Tau are conserved in the adult (mouse) brain. This evidence concerns the gene ACAT1 and Alzheimer disease.