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). The gene discussed is ACLY; the disease is Familial prostate cancer.