We next turned towards PKR, which displayed a pattern of expression completely different from cystatin C (Fig. 4B ). As expected from its IFN-inducible transcription, levels of PKR were increased in poly I:C-treated MEFs (Fig. 4B) , despite the strong global translation inhibition observed in these cells (Fig. 3) . GADD34 inactivation appeared to influence the accumulation of PKR, since the cytoplasmic dsRNA sensor levels were not upregulated and even decreased in poly I:C-treated GADD34 DC/DC MEFs (Fig. 4B ). Control treatment with tunicamycin and thapsigargin did not alter significantly PKR levels (Fig. 4B) , suggesting that ER stress did not influence the kinase expression. The absence of PKR up-regulation in the poly I:C-treated GADD34 DC/DC MEFs led us to investigate the capacity of these cells to produce anti-viral and inflammatory cytokines, which normally drive PKR expression through an autocrine loop. We ruled out any interference from the UPR in triggering IFN-ß production in our experimental system, since, as anticipated from PKR expression, tunicamycin and thapsigargin treatments were not sufficient to promote cytokine production in MEFs (Fig. S6 ) [43, 44] .