Prostate cancer cells therefore use three independent mechanisms to control AR levels: LSD1-mediated transcriptional repression of AR (Cai et al, 2011), E3-mediated degradation of ligand-free AR (An et al, 2014; Li et al, 2014; Lin et al, 2002; Qi et al, 2013; Sarkar et al, 2014), and ADP-ribosylation-dependent degradation of androgen-bound AR in association with chromatin. This evidence concerns the gene AR and prostate cancer.