G-6-PD deficiency is frequently associated with neonatal hyperbilirubinemia, which may be severe enough to cause kernicterus and death. Because of its association with acute trigger-induced hemolytic crises, G-6-PD deficiency-associated neonatal hyperbilirubinemia has been labelled as hemolytic in origin. In this article, the authors summarize recent evidence demonstrating that hemolysis cannot in and of itself be responsible for jaundice and that decreased bilirubin elimination plays a major role in its pathogenesis.