In summary, deletion or inactivation of the MR gene attenuates left ventricular dilatation, cardiac hypertrophy, and heart failure progression, whereas overexpression of the MR in cardiomyocyte-specific MR overexpression promotes cardiac adverse remodeling, heart failure progression, and development of arrhythmias [27,29,36]. This evidence concerns the gene NR3C2 and Arrhythmia.