The increased phosphorylation of PERK and eIF2α, upregulation of CHOP signaling in temporal cortex, increased expression of BiP chaperones, HSP70 family proteins and increased splicing of XBP1 in temporal cortex and hippocampal tissue indicates increased UPR and chronic ER stress during AD pathology [349,350,351]. The gene discussed is EIF2AK3; the disease is Alzheimer disease.