In another study, utilization of the recently developed BE system (A3A(N57Q)-BE3) to introduce a point mutation on the +58-DHS of the BCL11A erythroid enhancer reestablished the globin chain balance in both thalassemic and SCD patient-derived HSPCs and reduced sickling of SCD-derived HSPCs [139]. This evidence concerns the gene BCL11A and Schnyder corneal dystrophy.