Telomeres have to be protected from being recognized as DNA damage by the repair machinery (the so-called 'end-protection problem'). This is mediated by the shelterin complex, and deletion of individual shelterin subunits has revealed that end-protection involves repression of signalling by ataxia telangiectasia mutated (ATM) and ATR, as well as inhibition of repair mediated by the non-homologous end-joining (NHEJ) and homology-directed repair (HDR) pathways. To definitively pin-point all pathways that are repressed by the shelterin complex, Sfeir and de Lange generated mouse telomeres lacking all shelterin proteins and associated factors. They identified two additional pathways: alternative NHEJ (which was activated when Ku70–Ku80 was also absent) and nucleolytic degradation (which was activated when p53-binding protein 1 (53BP1) was also absent). So, telomeres are protected from six DNA repair pathways by the shelterin complex, which functions together with DNA repair proteins.