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Co-translational quality control is triggered as aresponse to translational stalling events. Yet, different molecular mechanisms are employed for the recognition of these stalls and to trigger downstream rescue and quality control pathways. While the recognition of individual stalled ribosomes is poorly understood, the use of collided ribosomes as a proxy for the recognition of translation problems in the cell is conserved from bacteria to humans1–3. In eukaryotes, co-translational quality-control processes triggered by ribosome collisions accomplish several tasks and eventually trigger stress response signalling pathways. grated stress response (ISR) is a highly conserved eukaryotic mechanism for integrating multiple signals to reprogram gene expression. These signals are conveyed by protein kinases that phosphorylate the α subunit of the initiation factor 2 (eIF2). Mammals have four known eIF2α kinases: GCN2, PERK, HRI, and PKR, which are activated in response to amino-acid starvation, ER stress, cytoplasmic protein misfolding and viral infection, respectively.