RECENT evidence indicates that sterol biosynthesis from acetate, but not from mevalonate, increases several-fold in the developing rat liver after weaning1. This increase parallels the postnatal rise in activity of liver 3-hydroxy-3-methyl-glutaryl-CoA reductase (HMG-CoA reductase), an enzyme which seems to catalyse the rate-limiting key reaction of hepatic sterologenesis both in the adult and in the developing rat2,3. Delayed weaning blocks the normal increase of HMG-CoA reductase which indicates that dietary factors are responsible for the observed changes, and rat milk was shown to contain an inhibitor of HMG-CoA reductase activity2.