The base editor is a RNA-protein complex, adapted from the CRISPR/Cas9 system and cytidine deaminase (Komor et al., 2016). The effector protein is composed of cytidine deaminase (rAPOBEC1), Cas9, and uracil DNA glycosylase inhibitor (UGI). It can deaminate cytidine (C) to uridine (U) without inducing DNA DSB, and finally result in C-to-T (or G-to-A) conversion in the target DNA sequence (Hohmann, 2017; Komor et al., 2016; Liang et al., 2015). Efficient base editing at single-base resolution has been reported in plant, yeast, human cells, mouse zygotes, and human tripronuclear zygotes (Chen et al., 2017; Kim et al., 2017b, c; Komor et al., 2016; Li et al., 2016, 2017a, b; Liang et al., 2017; Lu and Zhu, 2016; Ren et al., 2017; Zhou et al., 2017); Zong et al., 2017). Intriguingly, mouse embryos and pups with 100% point mutation efficiency (free of mosacism), as well as human tripronuclear zygotes has been generated (Kim et al., 2017c; Li et al., 2017a; Liang et al., 2017). However, whether base editors can repair homozygous T>C (or A>G) disease mutant in human embryos remains to be tested.