Previous studies have shown that the editing of either BCL11A (mutating GATA1 binding motif) or HBG1/2 loci (mutating BCL11A binding motif) can induce the upregulation of fetal hemoglobin (HbF) and thus could be a promising therapeutic strategy for treating sickle cell disease (SCD) and β-thalassemia (Supplementary Fig. 22)45,46. Here, BCL11A is linked to Schnyder corneal dystrophy.