Interestingly, an enhancer element was discovered that specifically coordinates BCL11A in erythroid cells and inactivation of this enhancer by gene editing leads to suppression of BCL11A and upregulation of γ-globin only in cells of the erythroid lineage.30,31,263 Thus, this approach provides both a mechanism of gene-editing therapy for sickle cell disease and β-thalassemia, but more broadly suggests a general strategy of therapeutic modulation of gene expression through the targeted editing of cell type-specific enhancers. Here, BCL11A is linked to sickle cell disease.