Most of longevity genetics has been asking a static question about a dynamic system. Arends, Ashbrook, and Williams tracked 6,438 mice from puberty to natural death, published in Nature. The core finding is not a list of longevity genes. It is that the same genetic variant can extend life at one age and shorten it at another. The polarity of the effect flips across the lifespan. This is a systematic pattern across 59 well-defined loci, built from two decades of data. We may have underestimated genetics in aging partly because of how we measured it. Standard mapping treats lifespan as a single number, so a gene that only affects mortality after day 900 is invisible. This team remapped it 72 times in progressively older survivor cohorts. What emerged includes genetic interaction networks that are almost entirely sex-specific (78 epistatic links in males, 72 in females, only 2 overlap) and at least one locus, APEH, that replicated in humans through Mendelian randomization against UK Biobank. This is the genetic layer upstream of what aging clocks measure. Clocks read where your trajectory is right now. This paper starts to map what programs it. 🧬