Over the last decade, epidemiological, experimental and clinical studies have in fact implicated oxidative stress in the development and progression of prostate cancer.47 A possible explanation identifies in the oxidative stress the key factor responsible for the activation of androgen receptor signaling and for the pro-survival and antiapoptotic effects in response to androgen-deprivation therapy, as well as to cytotoxic and tumor-suppressive interventions.48 The gene discussed is AR; the disease is neoplasm.