Knocking out a single gene can more than double the life expectancy of a small worm. Over the past two decades, scientists have uncovered scores of single mutants that increase lifespan in laboratory organisms. But in the case of aging, the links between genotype and phenotype are extremely complex. On closer inspection, the molecular basis of aging involves a large and complex network of genes, proteins and metabolites. In fact, a comprehensive understanding of the genetics of aging calls for an integrated approach, linking not just genes or proteins in molecular networks, but a suite of molecular, behavioral, physiological and demographic traits, from single cells to large populations. Recognizing this complexity, Dr. Promislow's work on the evolution of aging attempts to answer two key questions. First, why is there variation rates of aging among individuals, and second, why do different processes fail at different rates within individuals? Here, he will describe how a network approach, applied to inbred, laboratory models as well as to genetically heterogeneous populations, can shed new light on these important questions.