To overcome this limitation, we first tried to knock in a mutated sequence of CTNNB1 exon 3 to human HCC cells with the help of the CRISPR/Cas9 system by using single strand DNA or plasmid donor, but it is difficult to obtain CTNNB1-mutated subclones because homology-directed repair is less dominant than non-homologous end joining (NHEJ) during double-strand break repair. Here, CTNNB1 is linked to hepatocellular carcinoma.