HBG1 and Schnyder corneal dystrophy: Nuclease-based GE strategies for the treatment of SCD include (1) the correction of disease-causing mutation and (2) the reactivation of γ-globin genes (HBG1/2) that are normally silenced soon after birth,10 as a genetic condition causing hereditary persistence of fetal hemoglobin (HPFH) in adulthood ameliorates the SCD clinical phenotype.11