To validate the synthetic lethal interaction observed between mitochondrial metabolism and MYC inhibition, we focused on two key hits from our screen using the MycCaP castration-resistant prostate cancer cell line: Ndufa3, a core subunit of complex I (30), and Sod2, a mitochondrial superoxide dismutase that protects against oxidative stress (31). This evidence concerns the gene MYC and prostate cancer.