Aging is accompanied by a gradual decline of cell proliferation potential, associated with repressed expression of the transcription factor FOXM1, involved in cellular proliferation and cell cycle progression. Ribeiro et al. show that cyclic expression of a truncated form of a FOXM1 transgene in vivo can delay senescence-associated progeroid and natural aging phenotypes in mice, ultimately leading to healthspan and lifespan extension. These observations have added a beneficial role of FOXM1 as a potential driver of organismal rejuvenation.