In summary, transduction of CD34+ cells from patients with β-thalassemia and SCD with HDAd-EF1α.ABE8e mediated efficient editing of the HBG1/2 target site and the reactivation of γ-globin expression, resulting in phenotypic amelioration of erythroid cells after in vitro ED of HSCs. The gene discussed is CD34; the disease is Schnyder corneal dystrophy.