Correction of IVS I-110(G>A) β-thalassemia by CRISPR/Cas- and TALEN-mediated disruption of aberrant regulatory elements in human hematopoietic stem and progenitor cells

β-Hemoglobinopathies result from mutations in the β-globin ( HBB ) gene.[1][1] Whereas causative mutations may be corrected by precise gene correction based on homology-directed repair, imprecise disruption of genome elements by non-homologous end joining is inherently more efficient and more