BCL11A and thalassemia: Lentiviral-mediated KLF1 knockdown of normal (n = 3) and HbE/β0-thalassemia (n = 3) erythroblasts revealed that the expression of the γ–globin gene suppressor BCL11A decreased due to the absence of KLF1, which in turn activates the γ–globin gene and elevates HbF levels.