Prostate cancer (PCa) is the most common cancer in American men. Even though the 5-year survival rate for localized and regional PCa is 100%, the 5-year survival rate for patients with distant metastasis is only 31%, suggesting there is an urgent need to understand the underlying mechanisms that drive advanced prostate cancer to discover new therapies.1 Dysregulated lipid metabolism is a major hallmark of prostate cancer, which is associated with poor prognosis.2 Major oncogenes of prostate cancer enhance lipid synthesis by increasing the expression of fatty acid biosynthesis enzymes.3 Acetyl-CoA is the precursor molecule for lipid synthesis, which is formed by breaking down citrate. Citrate is produced in the mitochondria and then exported into the cytosol for lipid synthesis. Thus, to support the increased lipid synthesis, mitochondria of the prostate tumors must increase the production of citrate. Although we know several transcriptional factors activate the enzymes to increase lipogenesis, it remains unclear how these nuclear factors communicate with mitochondria to increase citrate synthesis to provide building blocks for lipogenesis.