In Alzheimer’s and Parkinson’s diseases, the accumulation of misfolded proteins, such as amyloid-beta (Aβ) and alpha-synuclein, can induce ER stress and activate the unfolded-protein response (UPR) via three independent ER stress pathways: inositol-requiring enzyme 1 (IRE1), activating transcription factor 6 (ATF-6), and protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK). This evidence concerns the gene ATF6 and Parkinson disease.