DDIT3 and neoplasm: Using mouse embryonic fibroblasts, Chitnis et al. [17] found that miR-211 is a pro-survival molecule that is expressed in a PERK (aka EIF2AK3, Eukaryotic translation initiation factor 2-alpha kinase) -dependent manner and regulates the expression of chop/gadd153 by mediating temporal accumulation of the pro-apoptotic transcription factor chop. PERK is important to survival of tumor and normal cells in response to stress [18-22] and Chitnis et al. [17] suggested that miR-211 negatively regulates chop accumulation, allowing cells to re-establish homeostasis before having to commit to apoptosis.