The findings summarized in this review provide experimental evidence that the aberrant activation of eIF2α phosphorylation pathways found in AD may be responsible for multifaceted memory-deteriorating and neurodegenerative mechanisms, including accelerated β-amyloidogenesis through BACE1 elevation, CREB dysfunction via ATF4 upregulation, and inhibition of general translation (Figure 1). The gene discussed is ATF4; the disease is Alzheimer disease.