The ribonucleoprotein telomerase is known to extend the replicative lifespan of cells by counteracting telomere shortening. However, evidence is emerging that telomerase might also promote cell survival through other, telomere-independent, mechanisms – perhaps by enhancing resistance to oxidative stress. On page 1046, Gabriele Saretzki and colleagues describe one such mechanism. Using human fibroblasts that overexpress TERT (the catalytic subunit of telomerase), the authors show that TERT cannot slow telomere shortening in response to hyperoxia; instead, TERT translocates from the nucleus and localises to mitochondria. The authors go on to show that TERT protects mitochondria from hyperoxia-induced damage on a number of fronts: mitochondrial DNA damage and superoxide production both decrease in cells that express the TERT transgene, and the mitochondrial membrane potential is elevated. Moreover, the transfected cells have enhanced resistance to apoptosis. The direct action of telomerase on mitochondria might, the authors propose, be an important protective function of the enzyme.