Erythrocytes from newborns have altered lipid composition and organization across the membrane bilayer. There does not appear to be any major difference in the protein profile of the membrane in neonatal and adult erythrocytes. The erythrocyte membrane of newborns is particularly susceptible to oxidative damage presumably due to low vitamin E and reduced activities of antioxidative enzymes. Neonatal erythrocytes have reduced membrane fluidity and shortened survival even though cord blood may have a relatively young population of erythrocytes. Shortened survival can be caused by a combination of factors, such as differences in cell geometry, membrane lipid composition, immunoglobulin binding to the surface, and membrane oxidative damage. Some of these factors may be developmental whereas others may be related to the vulnerability of neonatal erythrocytes to in vivo oxidative stress. Vitamin E deficiency in the newborn period is well documented; however, this conclusion is based on plasma vitamin E levels. Whether or not erythrocytes of newborns also exhibit vitamin E deficiency needs investigation. It is not known if the most dense, presumably senescent, erythrocytes are the ones most susceptible to membrane oxidation and are therefore major contributors to altered membrane lipid organization across the membrane bilayer and to hypercoagulability in the newborn period. Whether or not changes in the phospholipid organization in neonatal erythrocytes are developmental or are related to the vitamin E deficiency of newborns is not known.