Studies employing pharmacological and genetic manipulation of key regulatory enzymes of lipid metabolism in immortalized cell lines and xenografts have demonstrated the importance of several lipid metabolism pathways in prostate cancer progression including increased de novo lipogenesis (i.e., via ACLY, ACC and FASN inhibition) (73–76), triacylglycerol storage (DGAT1) (77), cholesterol metabolism (SOAT1, HMGCS1, HMGCR, and SCARB1) (78–80), lipolysis (MAGL) (81), and fatty acid elongation (ELOVL5 and ELOVL7) (82, 83). This evidence concerns the gene ACLY and prostate carcinoma.