Resistance mechanisms of prostate cancers to HDAC inhibitor treatment comprise the upregulation of detoxifying P-glycoprotein (P-gp) transporters, increased expression of HDAC enzymes, suppression of HAT enzymes, and upregulation of tumorigenic p21 (p21 is usually a tumor suppressor, but oncogenic functions of p21 were reported upon HDAC treatment)[24]. The gene discussed is HDAC9; the disease is prostate carcinoma.