Amelioration of the beta-thalassemia or sickle cell phenotype by increasing HbF levels has been extensively proven, and key regulators of γ-globin gene (hemoglobin subunit gamma 1/2 [HBG1/2 [MIM: 142200/142250]) expression, such as BCL11 transcription factor A (BCL11A) or zinc finger and BTB domain-containing 7A (ZBTB7A/LRF), have been identified [14,15,16,17,21]. The gene discussed is HBG1; the disease is beta thalassemia.