Furthermore, CRISPR-Cas9 disruption of the ZBTB7A binding sequence within the HBG1/HBG2 promoters in SCD patient-derived HSPCs efficiently reactivated γ-globin expression, restored globin chains imbalance and improved SCD phenotype [144] (Table S2). This evidence concerns the gene ZBTB7A and Schnyder corneal dystrophy.