In ADAR1-containing cells, PKR autophosphorylation is suppressed following viral infection, but in ADAR1-deficient cells it is enhanced because of the lack of editing-mediated destabilization of dsRNA, lack of sequestration of dsRNA by ADAR1 and also because of a lack of formation of inactive heterodimeric ADAR1:PKR complexes [4]. Here, EIF2AK2 is linked to viral infectious disease.