There is a high level of erythropoiesis in the growing fetus. In utero relative hypoxia results in a relatively high haematocrit and predominant synthesis of haemoglobin F, with erythropoietin (EPO) produced in the liver regulating erythropoiesis. At birth after full-term pregnancy, fetal EPO concentrations are high, but decline progressively thereafter. In pre-term infants the expected postnatal decline in haemoglobin is more prolonged than in full-term infants and the premature infants may become anaemic. It has been shown in a randomized, double-blinded, placebo-controlled trial that recombinant human erythropoietin (r-HuEPO) at a dose of 100 U/kg given intravenously twice weekly for 6 weeks to infants with anaemia of prematurity produced an earlier increase in reticulocyte counts compared with placebo; however, the difference between treatments was not significant. r-HuEPO therapy did not suppress subsequent release of endogenous EPO. It is concluded that a higher dose of r-HuEPO may be required to treat anaemic premature infants.