Furthermore, a different group performed in vivo prime editing of beta-globin using a nonintegrating HDAd-PE5max vector after HSC mobilization in the SCD mouse model CD46/Townes, and obtained 40% editing of beta-globin S alleles in HSCs (Table 1), 43% replaced hemoglobin, reduced SCD phenotypes, 1.5% on-target indels, and no detectable off-target edits [71]. Here, HBB is linked to Schnyder corneal dystrophy.