Myocardial angiotensin II levels were similar between groups, suggesting that HDAC-inhibition reverses atrial fibrosis, Cx40 remodeling and atrial arrhythmia vulnerability, rendering the atrium almost refractory to arrhythmia inducibility, independent of angiotensin II in cardiac hypertrophy (Liu et al., 2008). The gene discussed is AGT; the disease is cardiac arrhythmia.