Colorectal is the third most common cancer diagnosed in the United States. It is also the third leading cause of cancer-related deaths in men and in women. Current treatments for colorectal cancer includes surgery, chemotherapy, and radiation. However, these therapeutics are limited in preventing the progression of the disease and attacks both cancerous and healthy cells. Thus, more targeted therapeutics are needed. Advances in human genome studies have found that gene alterations are key in the treatment of cancer. WRN is a RecQ DNA helicase that is a lethal target for cancer cells with microsatellite instability (MSI), a mutation that results in impaired mismatch repair. MSI cells that are depleted of WRN undergo cell cycle arrest and/or apoptosis due to DNA double-strand breaks. Previous iPOND experiments conducted by the Brown Lab found multiple proteins were recruited to the replication fork following WRN depletion in cells. This project chose to knockout one of the recruited proteins, referred to as geneX, in the human colon cancer cell line RKO. This was done via the CRISPR-Cas9 mechanism. We hoped to observe a synergistic effect between WRN and GeneX in cancer cell death as measured by flow cytometry. The results found that the knockout of solely GeneX in RKO cells results in cell death. We also did not observe a synergistic effect between WRN and geneX suggesting that geneX itself is a lethal target for RKO cells. These findings support the development of therapeutic agents that target specific genes in MSI cells.