Mutations in the metabolic enzyme fumarylacetoacetate hydrolase (FAH) cause hereditary tyrosinemia type I (HT1) in human. HT1 patients present acute and irreversible liver and kidney damage during inf
Base editing, a method for correcting genetic mutations, has broad potential utility. Unlike traditional CRISPR-Cas9 homology directed repair (HDR), point mutations can be corrected without supplying