Recent studies of positive IGF-1 influence on lifespan showed that it is highly involved into the regulation of individual's longevity and response to oxidative stress. One more study just confirms recent results^*. Studies in invertebrates have led to the identification of a number of genes that regulate lifespan, some of which encode components of the insulin or insulin-like signalling pathways. Examples include the related tyrosine kinase receptors InR (Drosophila melanogaster) and DAF-2 (Caenorhabditis elegans) that are homologues of the mammalian insulin-like growth factor type 1 receptor (IGF-1R). To investigate whether IGF-1R also controls longevity in mammals, scientists have inactivated the IGF-1R gene in mice (Igf1r). In this study heterozygous knockout mice were used, because null mutants are not viable, and it was concluded that Igf1r^+/- mice lived on average 26% longer than their wild-type littermates (P < 0.02). Female Igf1r^+/- mice lived 33% longer than wild-type females (P < 0.001), whereas the equivalent male mice showed an increase in lifespan of 16%, which is not statistically significant. Long-lived Igf1r^+/- mice didn't develop dwarfism, their energy metabolism was normal, and their nutrient uptake, physical activity, fertility and reproduction were unaffected. The Igf1r^+/- mice displayed greater resistance to oxidative stress, a known determinant of ageing. Such results indicated that the IGF-1 receptor may be a central regulator of mammalian lifespan.