In contrast (and despite a degree of cytotoxicity), two cycles of electroporation led to BCL11A editing rates of ∼90% and therapeutically relevant HbF levels (∼30%) in SCD RBCs; full correction of the β+-thalassemic phenotype was achieved by combining BCL11A editing with correction of the disease-causing mutation51. This evidence concerns the gene BCL11A and Schnyder corneal dystrophy.