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Proteins of the BCL‐2 family are key mitochondrial actors in the intrinsic pathway of apoptosis. However, they also exert housekeeping functions at the level of the endoplasmic reticulum (ER), controlling Ca 2+ homeostasis and the unfolded protein response (UPR). Klee et al (2009) in an article published in this issue, identified that proapoptotic proteins of the BCL‐2 family can activate the mitochondrial pathway of death also when restricted only at the ER, by engaging an atypical arm of the UPR requiring Ca 2+ . This paper elucidates how unconventional cascades overcome the spatial restriction of cellular signalling components and add a further layer of complexity to the regulation of cell death.

When separation means death: killing through the mitochondria, but starting from the endoplasmic reticulum