Ovarian clear cell carcinoma (OCCC) is the most lethal gynecological cancer. It is characterized by somatic inactivating mutations of ARID1A, a component of the SWI/SNF chromatin-remodeling complex, occurring in up to 70% of patients. Patients with these mutations in their tumors have considerably poorer outcomes compared to those without such mutations. ARID1A-deficient cells have been shown to have a higher dependence on mitochondrial respiration, suggesting that targeting mitochondrial respiration is a promising approach to eliminating ARID1A-deficient cancer cells. Here we generated and characterized OCCC-derived ARID1A wild type and knock-out cell lines. Our proteomic data provide evidence of the increased relative abundance of mETC proteins in the ARID1A knock-out OCCC cells. Taken together, our data provides a rationale for identifying therapeutic vulnerabilities within the mETC in the context of treating ARID1A-deficient OCCC.