For this, we envision that, after obtaining appropriate IRB approval, human embryonal, fetal or neonatal hepatocytes would first be propagated in immuno-deficient mice that lack the enzyme fumarylacetoacetate hydrolase (Fah), and that serve as a model for type 1 hereditary tyrosinemia [216,217,218]. The gene discussed is FAH; the disease is tyrosinemia.