In vivo animal studies have shown that 2-week treatment with the hydroxamic acid, pan-HDAC inhibitor, trichostatin A (TSA), or valproic acid can either block the development of cardiac hypertrophy in transgenic mice that overexpress an HDAC2-dependent SRF inhibitor, Hop (homeodomain-only protein) (118), no matter what strategy of cardiac hypertrophy inducing, including continuous infusion of isoproterenol or Ang II, and pressure-load model due to TAC (6, 118). The gene discussed is HOPX; the disease is persistent truncus arteriosus.