CRISPR/Cas9-mediated editing and NHEJ successfully impaired mutant AAT and effectively ameliorated liver fibrosis in a humanized mouse model, thus supporting a potential therapeutic possibility of treating AATD patients.55 An additional study utilized coinjection of a dual adeno-associated vector (AAV): one encoding Cas9 and another expressing an AAT gRNA and an HDR donor template into the liver of a transgenic mouse model. This evidence concerns the gene SERPINA1 and alpha 1-antitrypsin deficiency.