Among this year's highlights in vertebrate aging research, we find a study in which, contrary to the oxidative stress hypothesis of aging, reduced expression of a major cellular antioxidant, glutathione peroxidase 4, led to a small increase in mouse lifespan. By contrast, a large comparative proteomic analysis discovered a remarkably robust and previous unsuspected inverse association between species lifespan and relative frequency of cysteine residues in mitochondrially encoded respiratory chain proteins only, which the authors attribute to cysteine's ease of oxidation. Another study evaluated more cleanly than any previous work the hypothesis that blood glucose concentration is a key mediator of aging, and concluded that it wasn't. Several new mouse longevity mutants were also reported this year, some (PAPP-A, IRS-1, and IRS-2 knockouts) supporting previous work on the importance of insulin/insulin-like growth factor-1 signaling and aging. However, there were inconsistencies between laboratories in some of the results, which merit further investigation. Also, somewhat inconsistent with these findings, over-expression of insulin-like growth factor-1 in heart only lengthened life. From a completely new direction, type 5 adenylyl cyclase knockout mice were observed to live more than 30% longer than controls. Finally, a new program for evaluating potential pharmaceutical interventions in aging and longevity made its appearance, and is notable at this point chiefly for the excellence of its experimental design. A similar program for the disinterested evaluation of reported longevity mutations in mice would be a service to the community of vertebrate aging researchers.