Benign prostatic hyperplasia is the most common benign neoplasia in men over 60 years of age, while prostate cancer affects 15 to 30% of men between 50 and 70 years of age. The clin­ical data suggest that androgens have an important role in the development of these diseases: patients with genetic defects in androgen biosynthesis and action never develop benign hyperplasia and prostate cancer. The pathogenesis of benign hyperplasia and prostate can­cer involves epigenetic and genetic changes, and includes several gene polymorphisms that are involved in the biosynthesis and action of androgens. In the prostate, the potent androgen 5a-dihydrotestosterone is formed both from testosterone and from inactive androgen precursors of adrenal origin. It then acts through the androgen receptor, stimulating the pro­liferation of the prostate epithelium and stroma and potentially leading to benign hyperplasia, while enhanced proliferation can increase DNA replication and the probability of genetic errors that result in prostate cancer. Androgen independent prostate cancer develops by several mechanisms: hypersensitivity or promiscuosity of androgen receptors, ligand independent activation, androgen independent pathways and selection of neuroendocrine cells. Androgen dependent prostate diseases can also be treated with agents that block androgen formation and action. Patients with hormone independent forms of prostate cancer are currently treat­ed with chemotherapeutics, while those therapeutics which inhibit the signalling pathways involved in the development of hormone independent disease are in the final phases of clin­ical trials. A better understanding of the molecular basis of these two diseases will help identify molecular markers and novel drug targets in the future, providing better diagnostics and a real possibility of individual patient oriented treatment.