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Tissue oxygenation in the fetus depends on fetal hemoglobin (HbF), but, shortly after birth, a switch to adult-hemoglobin production occurs. In individuals with sickle cell disease or β-thalassemia, adult-hemoglobin production is impaired. Thus, interventions that enhance HbF production during adulthood would ameliorate the severity of these diseases by partially compensating for diminished production of adult hemoglobin. Certain drugs, such as hydroxyurea and inhibitors of histone deacetylases, raise HbF levels; however, concerns about the safety and effectiveness of these agents have been raised. To explore whether physiologic regulation of HbF formation could lead to more-effective therapies for hemoglobinopathies, investigators studied …