These mice are ideal tools for this purpose because the lack of Fah results in metabolite accumulation that induces hepatocyte apoptosis, eventually leading to spontaneous liver failure if these mice are not supplemented with NTBC (2-[2-nitro-4-tifluoro-methylbenzyol]-1, 3-cyclohexanedione), an agent that blocks HPPDO upstream of Fah and prevents metabolite accumulation18. This evidence concerns the gene FAH and liver failure.