It is not clear, however, if either loss of negative feedback by differentiated prostate cancer cells on CSC proliferation or if therapeutic inhibition of the AR could contribute to increase the pool of prostate CSCs [3, 70, 71] or contribute to induction of EMT, epithelial mesenchymal plasticity and increased aggressiveness and reprogramming potential in prostate CSCs [5, 69, 72–74]. The gene discussed is AR; the disease is prostate carcinoma.