The incidence of prostate cancer in the United States has changed significantly compared with the 1980s and 1990s, and mortality due to this type of cancer has declined. In 2010, 217,730 new cases were diagnosed, with an expected mortality of 32,050, thus being the second leading causeofcancerdeath inmen(11%)(1).Afterprostatecancer progresses to metastasis, the standard first-line treatment is androgen-ablation therapy (usually by orchiectomy or a GnRH agonist), followed by the addition and, depending on the progression of the disease, subsequent withdrawal of an antiandrogen. The percentage of patients that benefit from this treatment is normally around 80 to 90%. After a few years, the disease becomes resistant to castration and develops into castration-refractory prostate cancer (CRPC) (2). Numerous research laboratories are focusing on correlation of genetic variants with the prognostic, diagnostic, or therapeuticoutcomeofprostatecancer.Theinvestigatorsare increasingly recognizing the importance of analyzing the metabolic pathway rather than a single gene. Prostate cancer is one of the many urological cancers that have been studied in this regard, and two genes have been outlined: estrogen receptor (ER ) and aromatase genes (3, 4). The estrogen receptors (ER and ER ) are ligand-activated transcription factors that belong to the nuclear hormone receptor superfamily activated by the sex hormone estrogen. The ER gene (ESR1) is mainly expressed in the uterus, prostate (stroma), ovary (theca cells), testes (Leydig cells), epididymis, bone, breast, various regions of the brain, liver, and white adipose tissue. The ER gene (ESR2) is expressed in the colon, prostate (epithelium), testis, ovary (granulosa cells), bone marrow, salivary gland, vascular endothelium, and certain regions of the brain. These receptors act as dimers and regulate the transcriptional activation by binding the DNA sequences that are primary targets for other transcription factors, such as cAMPresponsive elements and GC-rich Sp-1-binding sites (5). Aromatase, also called estrogen synthetase, is a member of the cytochrome P450 superfamily and is coded by CYP19 gene. The enzyme is capable of converting androgen to estrogen. The wide distribution of gene product suggests that estrogen produced by this enzyme has physiological functions not only as a sex steroid hormone but also in growth and/or differentiation (6). Studies in progress are aimed at defining the transcription mechanisms by which ER up-regulates CYP19 expression and activity; the involvement of the transcription factor Sp1 is suggested (7). It has been shown that ER can interact with MTA3, EGFR, HER2, and HER3 changing aromatase promoters activity (8). Estrogenic activity appears to involve, apart from the known classical pathway, newly discovered rapid membrane receptor mechanisms and possibly nonclassical nuclear ER-tethering pathways (9). Nowadays, selective estrogen synthetase inhibitors are considered to be promising tools in the control of some types of hormone-independent malignancies, including breast cancer (5). The most widely used cytotoxic chemotherapeutic agent that has currently been approved for the treatment of several types of cancer, in particular, hormone-refractory metastatic prostate cancer, is docetaxel. Docetaxel is a microtubule-polymerizing agent with well-established antimitotic chemotherapy action. However, in addition to