This leads to extensive repopulation of the liver with complete correction of the metabolic defect in the uridinediphosphoglucuronate glucuronosyltransferase 1A1 (ugt1a1)-deficient Gunn rat model of Crigler-Najjar syndrome type 1 (CN1) [16] and a mouse model of primary hyperoxaluria type 1 (PH1) [17]. The gene discussed is UGT1A1; the disease is primary hyperoxaluria type 1.