Using clustered regular interval short palindromic repeat-Cas9 gene editing to introduce variants into endogenous MSH2 sites in human embryonic stem cells, while eliminating wild-type genes, providing valuable information for determining pathogenic LS variants; using CRISPR/Cas9 system to introduce MSH2 mutations reported in the Lynch syndrome (LS) family into HeLa cells to study the phenotype of MMR deficiency. Here, MSH2 is linked to mismatch repair cancer syndrome 1.