However, to evaluate the role of eIF2α phosphorylation in Aβ-dependent BACE1 elevation in primary neuron culture and in the brain of the 5XFAD mouse model of aggressive amyloid pathology, Sadleir et al. used three genetic strategies: DNA damage-inducible 34 (GADD34) cytosine-adenine adeno-associated virus (CA-AAV) transduction, eIF2α S51A knock-in mutation, and BACE1-yellow fluorescent protein (YFP) transgene lacking upstream open reading frames (uORFs) in the 59 untranslated region (59UTR uORFs). This evidence concerns the gene BACE1 and amyloidosis.