Based on our finding that ECH decreased Aβ production by depressing BACE1 translation, we speculated that ECH treatment would inhibit Aβ-induced ERS and posttranscriptionally reduce the expression of BACE1 through inhibiting the activation of the PERK/eIF2α pathway in 2 × Tg-AD mice. This evidence concerns the gene EIF2AK3 and Alzheimer disease.