Likewise, in AD, GCN2 is a principal kinase shown to phosphorylate eIF2-α protein, blocking protein synthesis and arresting cell growth; conversely, eIF2-α phosphorylation induces the mRNA upregulation of BACE1 (a key enzyme involved in amyloid precursor protein (APP) processing to form Aβ) and ATF4, a repressor of long-lasting long-term potentiation (LTP) that influences synaptotoxicity in AD [62]. This evidence concerns the gene BACE1 and Alzheimer disease.