Many proteins ligands are shared between double-strand breaks and natural chromosomal ends or telomeres. The structural similarity of the 3' overhang, and the efficiency of cellular DNA end degradation machineries, highlight the need for mechanisms that resect selectively to promote or restrict recombination events. Here we examine the means used by eukaryotic cells to suppress resection at telomeres, target telomerase to short telomeres, and process broken ends for appropriate repair. Not only molecular ligands, but the spatial sequestration of telomeres and damage likely ensure that these two very similar structures have very distinct outcomes with respect to the DNA damage response and repair.