Cancer is a disease common to all complex life. Many life history traits, such as size and lifespan, are correlated with cancer risk between individuals of a species; however, this correlation does not hold when comparing between species. This phenomena, known as Peto’s Paradox, is resolved as species evolve cancer suppression mechanisms in parallel to increased sizes and lifespans. However, the exact mechanisms involved are largely unknown. Bats represent an ideal clade to study this paradox, as the large number of extant members - combined with the recent divergence time of the order - preserves a detailed record of the various genetic changes underlying their diversity in body size and lifespan. We show that the long-lived bat, Myotis lucifugus, has 8 copies of TP53, a central regulator of the DNA damage response present in all living organisms. Two of these copies - the canonical locus plus a second full-locus duplication - are unique to M. lucifugus, and show high levels of transcription in public RNA-seq and primary fibroblast data. To investigate how these two copies of TP53 influence the stress response of M. lucifugus relative to 4 other closely related bat species (M. evotis, M. thysanodes, M. yumanensis, and E. fuscus), we measured apoptosis, cytotoxicity, and viability in primary fibroblasts in response to chemically induced DNA-damage, unfolded protein response, and oxidative stress. We show that these two copies of TP53 play a role in mediating M. lucifugus’s unique response to these stresses relative to the other bat species. These results contribute to our understanding of how pre-existing tumor suppressor mechanisms have been enhanced through gene duplication to resolve Peto’s Paradox in large, long-lived organisms.