The etiology of the pediatric patients facing end-stage liver failure is quite different from that of adults, with almost one-half having biliary atresia (cholestasis). Other less prevalent condi-tions include autoimmune and sclerosing hepatitis, organ failure due to drug toxicity, and metabolic disorders. Several single locus genetic causes exist, including Wilson disease, alpha 1-antitrypsin deficiency, familial cholestatic syndromes, and tyrosinemia. Large, non-resectable hepatoblastoma, and hepato-cellular carcinomas may also warrant a transplant. While the overall number of liver transplants performed in the US rose exponentially since its inception until leveling off to about 6300 procedures per year since 2005, the number of pediatric trans-plantations has remained almost unchanged at about 550 since 1990.1 The aims of liver tissue engineering are to develop mechanisms to support hepatic function during the wait for a suitable organ, develop cell-based therapies to permanently provide specific missing biochemical functions in existing organs, and develop methodology to provide tissue-engineered alterna-tives to donor organs