,24,25,26,27 It has been recently proposed to use the base editing technology to disrupt the GATA1 activator BS in the erythroid-specific BCL11A enhancer without creating InDels, and reactivate HbF in the progeny of SCD and β-thalassemia patient HSPCs.16 The gene discussed is BCL11A; the disease is Schnyder corneal dystrophy.