This hypothesis emerges from comparative longevity research showing that bats defy the standard longevity-body size relationship. Where most mammals follow a predictable curve—larger means longer-lived—bats are dramatic outliers. Brandt's bat weighs ~7 grams but lives 41 years in the wild. A similarly sized mouse lives 3-4 years.The mechanism likely centers on DNA repair adaptations that evolved alongside flight. Flying is metabolically expensive and generates reactive oxygen species. Bats that could not manage oxidative damage would not survive. This created strong selection pressure for enhanced repair mechanisms that incidentally extended lifespan.Key evidence: Seim et al. (2013) showed Myotis bats have unique DNA repair gene expansions, including multiple copies of DNA-PKcs involved in double-strand break repair. Foley et al. (2018) demonstrated enhanced base excision repair in long-lived bat species compared to short-lived mammals.The flight-longevity hypothesis suggests an evolutionary tradeoff. Bats needed robust DNA repair to survive flight metabolism. Once evolved, these same mechanisms enabled exceptional longevity. This is antagonistic pleiotropy in reverse—selection for one trait (flight survival) produced another (extended lifespan) as a side effect.Testable predictions: 1) Bat fibroblasts will show faster double-strand break repair than mouse fibroblasts under oxidative stress. 2) DNA-PKcs knockout in bat cells will reduce lifespan more dramatically than in mouse cells. 3) Comparative transcriptomics will show upregulated BER and NHEJ pathways in long-lived versus short-lived bat species.Implications for human health: If bat DNA repair mechanisms can be characterized and mimicked, they may offer pathways to enhance human longevity without the complexity of modulating entire metabolic networks.