Cholesterol accumulation in prostatic tumors likely occurs by several mechanisms, such as an increased cholesterol uptake from the circulation, loss of feedback regulation due to downregulation of low density lipoprotein receptors, and an upregulation of specific components of the mevalonate (cholesterol synthesis) pathway, like the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase [23]. This evidence concerns the gene LDLR and prostate neoplasm.