Until now, the CRISPR-Cas9 system has been the preferred genome editing tool with a plethora of applications in many organisms for many purposes. However, there are still some limitations to this system, especially the “on-target” disruptive mutations caused by the NHEJ (non-homologous end-joining) repairing pathway, which is a dominant repairing mechanism for DSBs (double-strand breaks) caused by Cas9. Therefore, finding mechanisms to enhance the HDR (homology-directed repair) rate while simultaneously suppressing the NHEJ pathway is integral in increasing the gene editing efficiency of the CRISPR/Cas9 system. One method is creating a cell cycle-dependent Cas9 by fusing it with Geminin, a DNA replication inhibitor and a substrate of E3 ubiquitin ligase complex, which appears at the S and G2 phases while not presenting at other phases, resembling the working time of HDR in the cell cycle. In this study, we inserted a Geminin sequence into the Cas9 plasmid to create a Cas9-Geminin fusion construct, which is believed to express based on the cell cycle. Then, we assessed the fusion system on increasing gene editing efficiency by comparing the HDR efficiency of the fusion system with that of the original Cas9 system. Our initial results pointed out that the rate of HDR induced by the Cas9-Geminin system was significantly higher than that of the original Cas9. After this study, the data will guide future research toward achieving precise quantitative measurements and assessing the efficiency of the fusion system across various genetic loci. These efforts aim to further reinforce the effectiveness of CRISPR/Cas9-Geminin in gene editing.