In this study, we tested the hypothesis that genetic deletion of GCN2 may also reduce eIF2α phosphorylation that overly occur in brains of AD patients and a battery of APP transgenic mouse models [1]–[6], and thereby exert some beneficial effects on AD-like traits such as β-amyloidosis, CREB dysfunction and memory deficits. The gene discussed is EIF2A; the disease is Alzheimer disease.