FAH and Tyrosinemia type 1: Delivery of CRISPR/Cas9 components through the hydrodynamic injection or adeno-associated virus-9 have been applied to correct mutation of fumarylacetoacetate hydrolase (FAH) or dystrophin gene (dmd) in mouse models of hereditary tyrosinemia type I (HTI) or Duchenne muscular dystrophy through homologous recombination or exon skipping therapy [126–128].