In a different report, PE3 was microinjected into the zygotes of a mouse model for human beta-thalassemia IVS-II-654 mutation (C > T), which resulted in aberrant splicing of the beta-globin gene, with 14% editing efficiency (Table 1), restoration of normal splicing of beta-globin mRNA, and elimination of thalassemia symptoms [70]. Here, HBB is linked to thalassemia.