GADD34 has recently been shown to be necessary for the production of proinflammatory cytokines by dendritic cells and fibroblasts exposed to double-strand RNA in a murine model [14]. In fibroblasts, GADD34 expression is dependent on PKR (Protein Kinase RNA-activated) activation, showing a direct link between pathogen detection and the eIF2alphaP/ATF4 pathway of UPR. The importance of this link for anti-viral immunity has been demonstrated by the mortality of GADD34-deficient neonate mice infected by Chikungunya virus, due to a significant reduction of IFN-beta production [15]. It has been proposed that GADD34 could have a qualitative role on the selection of mRNAs being translated in particular conditions, such as viral infections [16]. These results suggest that GADD34 might be a key molecule of inflammatory processes in human pathologies as well; however, the role of GADD34 in cytokine production in humans remains to be elucidated. The aim of our study was to investigate GADD34 expression in RA patients.