The study identifies autophagy as a new effector mechanism in the process of cellular senescence. Autophagy is activated during senescence and its activation is correlated with negative feedback in the PI3K-mammalian target of rapamycin (mTOR) pathway. Overexpression of ULK3, a key autophagy-related gene, induces both autophagy and senescence. Inhibition of autophagy delays the senescence phenotype, including senescence-associated secretion. The data suggest that autophagy and its consequent protein turnover mediate the acquisition of the senescence phenotype. The study also examines the kinetics of autophagy regulation in oncogene-induced senescence (OIS) and finds that the delayed inactivation of mTORC1 activity correlates with the activation of autophagy and cell cycle exit. Additionally, the study shows that autophagy is required for the efficient production of senescence-associated secreted factors, such as IL6 and IL8, indicating that autophagy contributes to the establishment of the senescence phenotype.The study identifies autophagy as a new effector mechanism in the process of cellular senescence. Autophagy is activated during senescence and its activation is correlated with negative feedback in the PI3K-mammalian target of rapamycin (mTOR) pathway. Overexpression of ULK3, a key autophagy-related gene, induces both autophagy and senescence. Inhibition of autophagy delays the senescence phenotype, including senescence-associated secretion. The data suggest that autophagy and its consequent protein turnover mediate the acquisition of the senescence phenotype. The study also examines the kinetics of autophagy regulation in oncogene-induced senescence (OIS) and finds that the delayed inactivation of mTORC1 activity correlates with the activation of autophagy and cell cycle exit. Additionally, the study shows that autophagy is required for the efficient production of senescence-associated secreted factors, such as IL6 and IL8, indicating that autophagy contributes to the establishment of the senescence phenotype.