Hepatocytes have demonstrated that CRISPR/Cas9 can fix a Fah mutation in a mouse model of hereditary tyrosinemia type I. They co-injected single-stranded DNA (ssDNA) with Cas9, sgRNA, the wild-type G nucleotide, and homology arms flanking the sgRNA target area into the mouse model using a non-viral hydrodynamic injection. Here, FAH is linked to tyrosinemia type I.