Reduced Cx43 expression and its abnormal topology on the lateral sides of hypertrophied cardiac myocytes, as well as their disordered distribution in the fibrotic ventricles of rodents with HTN [19,26,80,81] or with PAH [28,62,72,82,83,84], may underly arrhythmogenic setting [27], which promotes non-uniform anisotropy, conduction defects and re-entry [85,86,87,88], as well as ventricular mechanical dysfunction [89,90]. This evidence concerns the gene GJA1 and hypertensive disorder.