The mutations in the two genes have been shown to cause abnormal activation of the renin-angiotensin-aldosterone system (RAAS) with characteristic elevations in the systemic levels of renin, aldosterone, and angiotensin II, which eventually lead to potassium ion loss and sodium ion retention, left ventricular hypertrophy, and atrial fibrillation [22,23]. This evidence concerns the gene REN and left ventricular hypertrophy.