Although the primary PKR activator is dsRNA—produced during infection by several viruses and detected at low levels in mammalian cells—PKR is also activated by a variety of cellular stresses including cytokines, calcium stress, oxidative stress, endoplasmic reticulum stress, lipo-stress, amyloid-β (Aβ) peptide accumulation, polyanions such as heparin, and several drugs, or through the PKR-associated activator (PACT) [7]. This evidence concerns the gene EIF2AK2 and infection.