Cellular senescence is involved in tumour suppression, tissue repair and, as shown by Muñoz-Espín et al.5 and Storer et al.6, embryogenesis. In all three cases, senescent cells express the protein p21 and proteins associated with the senescence-associated secretory phenotype (SASP); they also exhibit senescence-associated β-galactosidase (SA-β-gal) activity. However, during tumour suppression and tissue repair, senescence depends primarily on the activity of the proteins p53 and p16INK4a, which are often induced as part of the DNA-damage response (DDR). By contrast, senescence during embryogenesis depends on p21, which is switched on by the transcription factors FOXO and SMAD. Senescent cells in the embryo also express p15.