In preclinical models of renal and castration-resistant prostate cancer, a low dose of histone deacetylases inhibitor (HDACi), entinostat, a class I/III HDAC inhibitor, in combination with IL-2 therapy or a survivin-based vaccine, inhibited tumor growth, reduced infiltrating regulatory T cells (Tregs) and increased the T effector (Teff) response7. This evidence concerns the gene HDAC9 and neoplasm.