The hepatic enzyme tyrosine aminotransferase, normally expressed in very low amounts until shortly after birth, is prematurely induced in foetal rats made diabetic by the administration of streptozotocin in utero. Similarly, the enzyme is precociously induced in foetuses if the circulating insulin concentration is artificially decreased by the administration of anti-insulin serum. These observations support the proposal that the natural decrease in plasma insulin, known to occur at birth, is a major contributor to the postnatal induction of tyrosine aminotransferase.