PKR (encoded in humans by the gene EIF2AK2) activation is mainly dependent on the presence of double-stranded RNA during a viral infection. dsRNA causes PKR to form dimers, resulting in autophosphorylation and activation. Once activated, PKR will phosphorylate eIF2α which causes a cascade of events that result in viral and host protein synthesis being inhibited. Other stressors that cause the activation of PKR include oxidative stress, endoplasmic reticulum stress, growth factor deprivation and bacterial infection. Caspase activity early on in apoptosis has also been observed to trigger activation of PKR. However, these stressors differ in that they activate PKR without using dsRNA.