Can mouse genetics teach us enough about the biology of aging to guide the search for anti-aging medicines that can delay late-life illness? Recent progress gives reason for optimism, with new data showing that changes in single genes can extend average and maximal life span by 40%. Mice with these genetic variants remain healthy, active, and cognitively intact at average ages that correspond to 110-120 years of human life span. Multiple lines of evidence now point to a hormone, IGF-I, as a key influence on life span, with low IGF-I levels associated with extended longevity in multiple model systems. The goal of this research is not gene therapy-we have no idea of what genes to change, how to change them, or what harm such changes might do-but instead to use insights from the cell biology and endocrinology of genetically long-lived mice and other species to help develop drugs that manipulate aging and thus postpone the many diseases and disabilities that are typically troublesome in old age. The complete conquest of cancer or heart disease would each lead to an increase of a mere approximately 3% in mean life span in humans, i.e. about a tenth of what can be accomplished, today, in laboratory animals of delayed aging. In this context the paltry commitment to research in biological gerontology (six cents per $100 of NIH funding, for example) seems worth reconsideration.