Type I hereditary tyrosinemia is mainly caused by the mutation of FAH gene (fumaryl acetoacetate hydroxylase, FAH), which normalizes fumaric acid and acetoacetate. Is it the inability to metabolize tyrosine? Acid recessive genetic disease? With the development of gene editing technology for kidney damage and even liver cancer, we have successfully produced Fah transgenic mice, rats, rabbits and mini pig models. These animal models are now widely used in humans. HT1 disease research? Liver biology? Not only for liver stem cell and hepatocyte gene therapy research, but also for the preparation of humanized liver and human hepatocyte expansion bioreactor? This article is a type I inheritance, suitable for tyrosine blood.