To examine normal proliferation, they employed a mouse model of Type I hereditary tyrosinemia in which animals lacking fumaryl acetoacetate hydrolase (FAH), the terminal enzyme in tyrosine catabolism, succumb to liver failure as they accumulate cytotoxic tyrosine catabolites [89] unless the more proximal enzyme p-hydroxyphenylpyruvate dioxygenase (HPD) is blocked by the drug 2-(2-nitro-4-trifluoro-methyl-benzoyl)-1,3-cyclo-hexanedione (NTBC). The gene discussed is HPD; the disease is tyrosinemia.