Taken together, our data highlight the tremendous potential of correcting homozygous disease and compound heterozygous mutations by base editing in human somatic cells and embryos. Although we did not achieve 100% repair in human embryos, we and other groups have reported 100% base editing in mouse embryos (Kim et al., 2017c; Liang et al., 2017). By injecting BE3 protein and optimizing the injection time of the base editors, 100% repair of disease mutations may be achieved, as reported in CRISPR/Cas9 system (Hashimoto et al., 2016). Injecting BE3 protein may also help to improve the specificity of base editing mediated gene correction in human embryos. Moreover, we observed G>C mutation, caused by base excision repair (BER), in human cells and embryos (Komor et al., 2016). Therefore, developing new methods to inhibit base excision repair is needed, such as adding chemical inhibitors and overexpressing UGI (Wang et al., 2017). Additionally, while we found no indel formation in the cloned human embryos, indels have been observed in base editing in human cells and mouse embryos (Kim et al., 2017c; Komor et al., 2016; Liang et al., 2017). Further investigation is needed to block indel formation to improve the safety of base editing. Whether BE2 will lead to fewer indel at the HBB −28 sites will need further investigation.