We show that knockdown of KLF1 in human and mouse adult erythroid progenitors markedly reduces BCL11A levels and increases human γ -globin β -globin expression ratios. These results suggest that KLF1 controls globin gene switching by directly activating β -globin and indirectly repressing γ -globin gene expression. Controlled knockdown of KLF1 in adult erythroid progenitors may provide a method to activate fetal hemoglobin expression in individuals with β -thalassemia or sickle cell disease. © 2010 Nature America, Inc. All rights reserved.
