The study showed that histone deacetylase 6 (Hdac6) deletion in mice slows HFpEF progression, and that a specific HDAC6 inhibitor, TYA-018, reverses existing cardiac hypertrophy and diastolic dysfunction in mouse models of HFpEF [113], suggesting that HDAC6 inhibition may be a therapeutic approach for HFpEF. The gene discussed is HDAC6; the disease is cardiac hypertrophy.