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Induction of Fetal Hemoglobin by Gene Therapy

Shortly after birth, fetal hemoglobin is replaced by adult hemoglobin in red cells, a process that reflects a developmental switch in the β-globin locus that favors the expression of β-globin and the suppression of γ-globin. Therapies that may abrogate this switch have long been pursued on the basis of observations that the persistence of fetal-hemoglobin production after birth mitigates the phenotypes of sickle cell disease and β-thalassemia major, as well as the absence of signs of either disease when fetal hemoglobin levels are high in utero or at birth.1,2 Pharmacologic inhibition of the globin developmental switch would require regular and . . .

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