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Insulin-like growth factor-II (IGF-II) is thought to be a major growth factor during fetal and neonatal development. Levels of IGF-II mRNA fall dramatically in the liver - the major site of endocrine production - between 18 and 20 days post-natally. No information concerning the control of gene expression post-natally has hitherto been available. Using Northern blotting and in-situ hybridization, we show here that cortisone acetate rapidly extinguishes IGF-II mRNA expression in the neonatal rat liver. The effect at putative autocrine/paracrine locations such as skeletal muscle and choroid plexus is much less marked or absent. The repression by cortisone acetate is discussed in the light of the available IGF-II gene sequence.