As our findings indicated a broad growth inhibitory effect of HDAC inhibition in preclinical prostate cancer models, we further explored the activities of the class I-selective HDAC inhibitors etinostat and romidepsin, class I/IV-selective HDAC inhibitor mocetinostat, and the pan-HDAC inhibitor vorinostat. This evidence concerns the gene HDAC9 and prostate carcinoma.