Aβ is produced from APP via sequential cleavages by β- and γ-secretases.1 Dysregulation of BACE1 is involved in AD pathogenesis, and inhibition of BACE1 reduces Alzheimer’s phenotypes.4,37,42 Our data showed that upregulation of MKP-1 inhibited APP and BACE1 expression, leading to a reduction in the amyloidogenic processing of APP to generate Aβ. This evidence concerns the gene BACE1 and Alzheimer disease.