A study published in *Nature* (479(7372): 232–236. doi:10.1038/nature10600) investigates the role of p16Ink4a-positive senescent cells in aging-related disorders. The researchers developed a transgenic mouse model, INK-ATTAC, to selectively eliminate p16Ink4a-positive senescent cells. They found that removing these cells in a progeroid mouse background delayed the onset of age-related phenotypes, including sarcopenia, cataracts, and fat loss, and reduced the progression of established age-related disorders. The study also showed that senescent cells contribute to tissue dysfunction through the secretion of pro-inflammatory factors, known as the senescence-associated secretory phenotype (SASP). The results suggest that clearing p16Ink4a-positive senescent cells can prevent or delay age-related diseases and extend healthy lifespan. The study demonstrates that the removal of these cells is technically feasible and does not cause significant side effects. The findings support the hypothesis that cellular senescence is a key driver of aging and that targeting senescent cells may be a promising approach for delaying aging-related disorders.A study published in *Nature* (479(7372): 232–236. doi:10.1038/nature10600) investigates the role of p16Ink4a-positive senescent cells in aging-related disorders. The researchers developed a transgenic mouse model, INK-ATTAC, to selectively eliminate p16Ink4a-positive senescent cells. They found that removing these cells in a progeroid mouse background delayed the onset of age-related phenotypes, including sarcopenia, cataracts, and fat loss, and reduced the progression of established age-related disorders. The study also showed that senescent cells contribute to tissue dysfunction through the secretion of pro-inflammatory factors, known as the senescence-associated secretory phenotype (SASP). The results suggest that clearing p16Ink4a-positive senescent cells can prevent or delay age-related diseases and extend healthy lifespan. The study demonstrates that the removal of these cells is technically feasible and does not cause significant side effects. The findings support the hypothesis that cellular senescence is a key driver of aging and that targeting senescent cells may be a promising approach for delaying aging-related disorders.