RECENT STUDIES1-4 indicate that the heritability of many adult-onset diseases, such as Alzheimer disease (AD), cardiovascular disease (CVD), and type 2 diabetes mellitus, is less than 40% and in the same range as the heritability of life span. These emerging findings suggest that noninherited environmental factors play a major causal role in age-related diseases and indicate limitations in applying information on common genetic polymorphisms to the diagnosis, treatment, and prevention of major diseases of aging. However, such limitations do not negate the importance of genetic research in understanding the molecular mechanisms of aging and its diseases. The identification of mutations in familial AD, Parkinson disease (PD), and other diseases has given important insights into the mechanisms in the more common sporadic forms of these diseases. Furthermore, comparative studies5 of aging have identified signal transduction pathways that regulate resistance to cellular damage and longevity in organisms ranging from yeast to mammals. These recent findings set the stage for developing new drugs to prevent multiple age-related diseases.