Normal somatic cells are capable of a limited number of divisions, after which they permanently withdraw from the cell cycle and enter into replicative senescence. Cells that suppress these mechanisms continue dividing, which leads to telomere shortening and genomic instability. In most cells, this will lead to replicative crisis, which was previously associated with the activation of cGAS–STING innate immunity signalling and cell death via autophagy. Cells that avoid this crisis may succumb to oncogenic transformation. How the shortened telomeres activate innate immunity signalling to drive efficient elimination of cells in crisis has been elusive. Nassour et al. now demonstrate a key role of the innate immunity sensor Z-DNA binding protein 1 (ZBP1) in the response to telomere shortening.