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In this issue,Wang et al.report on the generation of a non-human primate model of Hutchinson-Gilford progeria syn-drome(HGPS)using a base editor.Base editing is an emerging novel genome editing technique for modifying a single base pair at specific sites in the genome.Base editors(BEs)have two principal components,a catalytically inactive or single strand cleaving Cas-variant,which binds to the guide RNA and a nucleobase deaminase domain to convert specific base pairs at the target loci(Komor et al.,2016;Nishida et al.,2016;Gaudelli et al.,2017).Cytosine base editor(CBE)and adenine base editor(ABE)are two base-editors,which convert Cytosine-Guanine(C-G)to Thymine-Adenine(T-A)and A-T to G-C,respectively.Likewise,RNA base editor(RBE)was created by fusing nucleobase deaminases with the Cas13 protein,which allows for a base substitution of A to inosine(I)or C to uracil(U)in the targeted RNA(Cox et al.,2017).Recently,a dual base editor was developed that can catalyze both cytosine and adenine base conversions at the same time,broadening base editing capability(Zhang et al.,2020).