The fact that single-gene mutations can prolong an organism's lifespan might seem unlikely, but many 'gerontogenes' have been identified in model organisms that, when knocked out or over- or underexpressed, increase or decrease lifespan in the laboratory environment. These genes largely assort into several now-familiar pathways [1,2], many of which converge on the insulin/insulin-like growth factor I (IGF-I) signaling pathway, which in Caenorhabditis elegans includes daf-2, an insulin/IGF-I receptor homolog; age-1, which encodes a phosphatidylinositol 3-OH kinase (PI3K) at the top of the DAF-2-activated signaling cascade; and daf-16, a forkhead-family transcription factor that is inactivated by this cascade. Nevertheless, it is unclear whether the activities of these 'longevity pathways' are modulated during normal aging, and as such, their role in the process of senescent decline in wild-type individuals is uncertain. Several pathways with longevity phenotypes in knockout animals may not be relevant to normal aging; these include the insulin/IGF-1 pathway, the endoplasmic reticulum stress response mediated by the sirtuin SIR-2.1, and mitochondrial electron transport . Because of this, many researchers in the field suspect that aging is primarily driven by accumulation of cellular damage and not age-related gene (dys)regulation.In a recent paper in Cell , however, Yelena Budovskaya and colleagues in the labs of Stuart Kim and Tom Johnson have identified a circuit of GATA transcription factors that alters C. elegans longevity when knocked out or knocked down, and which also plays a role in regulating the changes in gene expression observed during normal aging. Moreover, this circuit helps determine lifespan. One of these factors, ELT-3, is required for the pro-longevity effects of reduced insulin/IGF-I-like signaling and dietary restriction, providing at last a potential link between these longevity pathways and the normal process of aging.Budovskaya et al.