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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

haematologica

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