Hydrodynamic injection of Cas9-expressing and Fah-MMEJ constructs into Fah−/− mouse livers, which are a model of hereditary tyrosinemia type I (HTI) caused by a deficiency in fumarylacetoacetate hydrolase due to mutation of the Fah gene, resulted in correction of the Fah gene in hepatocytes, which alleviated symptoms such as body weight loss and liver damage as well as prolonged the lives of the Fah-corrected mice63. This evidence concerns the gene FAH and tyrosinemia type I.