This model is a Fah gene knockout (Fah KO) mouse. The Fah gene in the mouse, which is homologous to the human FAH gene, has been knocked out using gene editing technology. Heterozygous Fah KO mice are viable and fertile. These mice can exhibit the typical characteristics of hereditary tyrosinemia type 1 (HT1), that is, the metabolic disorder of tyrosine in the body, leading to the accumulation of fumarate acetoacetate (FAA), which in turn causes hepatocyte damage. Homozygous Fah KO mice will die shortly after birth, manifesting as liver and kidney dysfunction, hypoglycemia, and significant changes in liver mRNA expression, and nitisinone (NTBC) is required to maintain their survival.