Abstract

During fetal development and the first 6 months of neonatal life, a complex pattern of globin gene expression occurs called the hemoglobin switch (Figure 1). After a brief period of embryonic globin gene expression, the γ-globin chain of fetal hemoglobin (HbF, or α2γ2) is predominantly expressed, then is progressively replaced by the β-globin chain of adult hemoglobin (HbA, or α2β2).2 This process is clinically important because the persistence or reactivation of HbF production can be highly beneficial in attenuating the severity of the symptoms of inherited β-globin gene disorders, such as β-thalassemia . . .

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