Several strategies employ genome editing to boost HbF expression, most directly by the introduction of activating mutations in the γ-globin promoter that abrogate binding of postnatal repressors (Fig. 4B).130,131 The most frequently modified target of genome editing for the ß-hemoglobinopathies is BCL11A. BCL11A encodes a transcription factor that is required to turn off γ-globin expression during the perinatal hemoglobin switch. This evidence concerns the gene BCL11A and hemoglobinopathy.