Nonoptimal fetal growth, leading to a small-for-gestational-age body size at birth, is commonly followed by compensatory growth after birth. This pattern of growth is associated with an increased risk for type 2 diabetes, especially when the compensatory phase begins around 3 to 4 years of age. Genetic factors are of major importance for the development of type 2 diabetes, but despite extensive research, the identification of the underlying genes has not been particularly fruitful. This article focuses on interactions between intrauterine growth and genes in relation to adult health outcomes based on findings from the Helsinki Birth Cohort Study. We have shown that the effects of the Pro12Pro and Pro12Ala polymorphisms of the PPAR-gamma 2 gene depended on the body size at birth. Those individuals who had a small body size at birth and were carriers of the Ala allele seemed to be protected against insulin resistance and type 2 diabetes in later life. These findings reflect gene-early environment interactions and can be attributed to the phenomenon of developmental plasticity.