In 2014, another study demonstrated that using the mouse model of hereditary tyrosinemia type 1 (HT1), CRISPR/Cas9 system could be used to successfully correct a mutation in post‐natal animals.105 They used the Fah59815B mouse model that harbours a homozygous G to A point mutation in the fumarylacetoacetate hydrolase (Fah) gene. Here, FAH is linked to Tyrosinemia type 1.