Aging is a changing process in organisms over time. This inevitable process is characterized by a progressive deterioration of physiological ability, leading to impaired function and increased vulnerability to death. The aging process was previously thought of as a passive process of tissues caused by damage to macromolecules of the cell, such as genomic DNA, proteins and lipids. An unprecedented advance in aging research over recent years, however, suggests that the process of aging is controlled, at least to some extent, by evolutionarily conserved genetic pathways and biochemical processes. Since the isolation of the first long-lived mutant in Caenorhabditis elegans (C. elegans), a number of reports have described various genes and genetic signaling pathways that regulate longevity in model organisms such as yeasts, worms, flies and mice. This paper showed that, in C. elegans, mutations that decrease the activity of DAF-2, the C. elegans homolog of the insulin/insulin-like growth factor-1 receptor, more than double the lifespan of the animal. This finding opened the door for us to understand how aging is genetically regulated.