We are interested in testing the effects of increasing the gene dosage of critical tumor suppressors in mice to evaluate the consequences on cancer, aging and general organismal fitness. The tumor suppressors p53 and p16/ARF are among the most important sensors of stress, their activation is meant to eliminate damaged cells and thus prevent the appearance of tumors. Aging has long been considered to be the result of the accumulation of cellular damage. Based on this, we have reasoned that improving the efficiency of these checkpoints should decrease the burden of damaged cells and therefore should delay aging. I will present data on the aging of mice with increased p53, or with increase p16/Arf, or with combined increase of the above tumor suppressors. Also, I will present data on the impact of p53 dosage on telomere-driven aging.