Moreover, previous studies reported that, SAHA was more efficient in terms of growth inhibition and induction of cell death in androgen-responsive cells [39], suggesting that a component of the activity of SAHA in prostate cancer cells relates to the presence of a functional androgen signalling axis and that HDAC inhibitors decreased AR protein levels without significantly affecting AR protein stability [40, 41]. This evidence concerns the gene HDAC9 and prostate carcinoma.