GADD34 and PKR are necessary to produce anti-viral cytokines during CHIKV infection, and probably other types of infection. PKR, ATF4 and GADD34 should therefore be considered as an essential module of the innate anti-viral response machinery. The importance of PKR in anti-viral type-I IFN responses has been the object of contradictory reports [30, 31, 66, 67] . Our observations, however, suggest that PKR function should be re-evaluated by integrating the impact of viral detection on cellular translation. In eIF2A/A and PKR 2/2 cells, cytokine transcription is induced normally following poly I:C detection by DExD/H box RNA helicases, while as expected in these cells, no eIF2a phosphorylation and subsequent host translation inhibition are observed. This lack of translation arrest in the absence of potent eIF2a phosphorylation allows for normal cytokine production during dsRNA detection, with no requirement for an operational GADD34 feedback loop. The importance of PKR and GADD34 for IFN-b and other cytokines production could therefore be directly linked to the efficiency of the cellular translation inhibition induced by RNA viruses, as exemplified here with CHIKV, which in MEFs strongly activates PKR and subsequent protein synthesis inhibition.