HDAC2 and atrial fibrillation: In addition, HDAC2, which was found to be inactivated by β-OHB in our study, is essential for promoting heart development and maintaining heart function,47–49 and downregulation of HDAC2 increases apoptosis in cardiomyocytes.42 Our in vitro assay showed that β-OHB inhibited HDAC2, with an IC50 of 2.4 mM, which is lower than the β-OHB concentrations observed in the human AF heart and in KD-fed and deep-fasted rats (i.e., ~3–4 mM).