The target of rapamycin (TOR) kinase plays an evolutionarily conserved role, from yeast to human, in controlling metabolic activity in response to intracellular cues and extracellular stimuli . It stimulates anabolic processes that engender cell growth and proliferation by increasing protein synthesis and lipogenesis. TOR also inhibits autophagy, which is a major catabolic process. Persistent activation of TOR causes an imbalance between anabolic and catabolic processes, resulting in the accumulation of damaging reactive oxygen species (ROS), which favors the development of age-related disorders. Indeed, the inhibition of TOR by the drug rapamycin increases organism life span and reduces the incidence of age-related pathologies . On page 1223 of this issue, Lee et al. report that sestrin proteins prevent excessive TOR activation and delay the onset of age-related pathologies through a negative-feedback mechanism .