have provideda direct link between HDAC inhibition and SUMOylation in both cardiomyocytes andfibroblasts that may help explain the beneficial effects of HDAC inhibitors inpreclinical models of heart failure.38 Of note, the protectiveinfluences of the HDAC inhibitors have a foil in the class’ baselinetoxicity, and it has therefore proven difficult to optimize the concentrations thatmay ultimately achieve maximal protection from OGD/ROG.39 Strategies including pulsedtreatment may be employed to mitigate such toxicity moving forward.40 Here, HDAC9 is linked to heart failure.