Dear Editor,rnGenetic inactivation or gene knockout (KO) has been a powerful method of elucidating gene function in mice.The traditional method of generating KO mice via targeting mouse embryonic stem cells through homologous recombination is labor-intensive and of low efficiency.The emergence of clustered regularly interspaced short palindromic repeat (CRISPR) technology greatly simplifies the method of gene targeting at a reduced cost and with high efficiency.In its simplest form, CRISPR editing comprises two components, a single guide RNA (sgRNA) and Cas9 protein.Upon finding the complementary sequence preceding a protospacer adjacent motif (PAM), this ribonucleoprotein (RNP) complex generates a double-strand break (DSB) three nucleotides upstream of the PAM.The DSB is then repaired via error-prone non-homologous end-joining (NHEJ).Alternatively, a third component may be used involving a single-strand or double-strand repair template engineered with nucleotide substitutions, deletions or insertions of new genetic material[1].The presence of such repair templates biases the reparation of the DSB via homology directed repair (HDR) processes.