BACE1 and Alzheimer disease: While our work suggests it is highly unlikely that eIF2α phosphorylation is responsible for increased BACE1 levels observed in Aβ42 treated primary neurons or 5XFAD brains, further investigation of this pathway is still relevant as p-eIF2α levels are elevated in the brains of AD patients [22] and could affect AD pathology through mechanisms other than BACE1 elevation.