Hyperbilirubinemia remains one of the most common and more important pathological conditions in the newborn. The possibility that low levels of serum bilirubin could be responsible for bilirubin encephalopathy in the small premature infant is of great concern for the neonatologist. In fact, premature newborns, as recognized more than 70 years ago by Y1ppo, are prone to develop hyperbilirubinemia. The so-called physiologic of developmental hyperbilirubinemia could be harmful for the small preterm infant, who is at risk of developing bilirubin encephalopathy in the presence of low plasma bilirubin concentrations. Current methodologies for suppressing severe neonatal jaundice include: 1) Attempts to stimulate liver conjugating enzymes by drugs, such as phenobarbital. 2) Attempts to degrade bilirubin "in vivo" by phototherapy. 3) Exchange transfusion. It is too soon to consider Sn-protoporphyrin as a drug for the prevention and treatment of neonatal hyperbilirubinemia. However, if it can be shown that the use of tin-protoporphyrin can serve as a safe and less costly alternate treatment, a considerable improvement in the management of neonatal jaundice will be achieved.