Several lines of evidence have suggested that during prostate cancer development, AR has a dual function as an oncogene42 and a tumor suppressor.43 Moreover, the transcription profiles of AR could be very different between androgen-dependent and -independent prostate cancers.24 Our current study supported the tumor suppressor role of AR by indicating an AR-KLF4 positive feedback loop, which can inhibit malignant phenotypes in AR-negative or androgen-insensitive prostate cancer cells (PC3 and RasB1). The gene discussed is KLF4; the disease is prostate carcinoma.