Cellular senescence is linked to pathological contexts such as tumour suppression, as well as ageing. Now, two studies reveal that senescence contributes to mammalian embryonic development in several contexts, which suggests that it has an essential conserved role in normal physiology. Muñoz-Espín et al. analysed in detail the mesonephros and the endolymphatic sac of the inner ear. Senescence in both embryonic structures depended on p21 (but was independent of p53) and was regulated by the transforming growth factor-β and PI3K pathways. Furthermore, loss of cellular senescence led to developmental abnormalities (despite partial compensation by apoptosis). Storer et al. focused on two signalling centres in embryonic patterning — the apical ectodermal ridge (AER) and the neural roof plate. Mice deficient in p21 had defects in embryonic senescence, AER maintenance and patterning. These authors also report that senescence in the AER is instructed by the underlying mesenchyme and involves ERK signalling. Both groups find that senescent cells ultimately undergo macrophage-mediated clearance and that this is vital for development.