This is perhaps associated with the fact that ATF4 upregulation “may not only act as the downstream effector of Aβ but also as an upstream initiator for the memory deficit and pathological hallmarks in AD (Wei et al., 2015).” An association is possible between ATF4 elevation and increased phosphorylation of tau, through Glycogen Synthase Kinase 3 (GSK-3) and Protein phosphatase 1 (PP1) kinases, and this could give rise to neuronal damage. This evidence concerns the gene ATF4 and Alzheimer disease.