The identification and study of long-lived mutant animals has provided valuable insights into the mechanisms that limit the life-span of organisms. Findings with the gene SIR2 suggest that the rate of aging can be regulated under certain conditions. Indeed, increased expression of SIR2 lengthens life-span by acting on biological processes that promote survival under conditions of scarcity. In addition, studies of mutant strains of Caenorhabditis elegans, in particular daf-2, clk-1, and isp-1 mutants, suggest that the biology of reactive oxygen species in the mitochondria and elsewhere might be the main determinant of life-span in this organism. Thus, the aging process may be more specific than previously anticipated on evolutionary grounds.