The ABE combines A‐to‐G base editing in the HBG1 and HBG2 gene promoters that regulate HbF expression, mimicking naturally occurring HbF‐inducing mutations and reactivating HbF expression through high‐level base editing to compensate for the lack of HbA in patients with SCD. The gene discussed is HBG2; the disease is Schnyder corneal dystrophy.