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Glab and colleagues examine in a recent paper apoptosis induced by some driverss ofendoplasmic reticulum (ER) stress. They conclude that in contrast to a previously publishedreport2, DR5/TRAIL-R2 and caspase-8 are universally dispensable in ER stress-inducedapoptosis. We argue here that their own data and other published reports indicate that inmany models, DR5 and/or caspase-8 are essential players in apoptosis mediated by theunfolded protein response (UPR), upon chronic ER stress

A role for caspase-8 and TRAIL-R2/DR5 in ER-stress-induced apoptosis