Under stress conditions (e.g., oxidative stress, viral infections, amino acid starvation, and ER stress), phosphorylation of eIF2α by one of several stress-activated kinases (e.g., heme-regulated inhibitor kinase (HR1), protein kinase RNA (PKR), general control non-repressible-2 (GCN2), and PKR-like ER Kinase (PERK) [1,2,3,4]) inhibits the GDP:GTP exchange reaction, depleting eIF2α-GTP-tRNAiMet, and inhibiting translation initiation [5]. This evidence concerns the gene EIF2AK3 and viral infectious disease.