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Current therapeutic strategies for sickle cell anemia are aimed at reactivating fetal hemoglobin.Pomalidomide,a third-generation immunomodulatory drug,was proposed to induce fetal hemoglobin production by an unknown mechanism.Here,we report that pomalidomide induced a fetal-like erythroid differentiation program,leading to a reversion of γ-globin silencing in adult human erythroblasts.