Recent results indicate that PKR participates to the production of IFN-a/ß proteins in response to a subset of RNA viruses including encephalomyocarditis, Theiler's murine encephalomyelitis, and Semliki Forest virus [31] . Even though IFN-a/ß mRNA induction is normal in PKR-deficient cells, a high proportion of mRNA transcripts lack their poly(A) tail [31] . As GADD34 induction by poly I:C was completely PKR-dependent, we wondered whether the phenotypes observed in PKR 2/2 cells and GADD34 DC/DC MEFs could be related. Oligo-dT purified mRNA extracted from cells exposed to poly I:C were therefore analyzed by qPCR. PolyA+ mRNAs coding for IFN-ß and IL-6 were equivalently purified and amplified from WT and GADD34 DC/DC MEFs (Fig. S9 ). This confirms that albeit the phenotypes of PKR 2/2 and GADD34 DC/DC cells might be linked, mRNA instability is not the primary cause of the cytokine production defect observed in GADD34 DC/DC . Taken together these observations suggest the existence of a specific mRNAs pool, encompassing cardinal immune effectors such as IFN-ß, IL-6, and PKR, which are specifically translated in response to dsRNA sensing and increased levels of P-eIF2a. This mRNAs pool requires GADD34 for their translation during the global protein synthesis shut-down triggered by dsRNA detection.