Although the evidence for the cytoprotective autophagy associated with androgen deprivation needs to be further validated via the pharmacologic and genetic inhibition of autophagy in different cell lines, and importantly, in vivo, using different tumor models [50] and physiologically relevant concentrations (in contrast to some studies mentioned earlier that used supraphysiological concentrations of AR antagonists), autophagy inhibition in prostate cancer likely has the potential to increase the efficacy of androgen antagonists. The gene discussed is AR; the disease is prostate cancer.