Altered RAS signaling is evident in hypertension [[7], [8], [9], [10], [11]], heart failure [[12], [13], [14]] and post-myocardial infarction [[15], [16], [17], [18]], where AngII-AT1R activation is involved in enhanced sympathetic transmission [[19], [20], [21]], cardiac hypertrophy [8,13,[22], [23], [24]] impaired calcium handling [9], vascular remodeling [3,4] and pro-inflammatory events [25,26] that all contribute to cardiac arrhythmia [27]. The gene discussed is AGT; the disease is hypertensive disorder.