The two best characterized models are the Alb-urokinase type plasminogen activator (uPA) transgenic mouse [88,89] in which sub-acute liver failure is induced by the uPA transgene and the knockout fumarylacetoacetate hydrolase (FAH) mouse model [90,91,92] in which hypertyrosinemia and liver failure ensue unless the animals are protected by consuming the NTCB drug. The gene discussed is PLAU; the disease is liver failure.