AGT and hydrops fetalis: The possible utility of HDAC6 inhibition for the treatment of HFrEF is underscored by the prior demonstration that HDAC6 catalytic activity is elevated in models of HF (43), and HDAC6 KO and/or tubastatin A administration improves systolic function in mouse models of pressure overload, angiotensin II infusion, doxorubicin treatment, and ischemia/reperfusion (22, 44, 45).