The pathogenesis of PA cardiomyopathy is now increasingly recognized as multifactorial, involving both traditional determinants, such as disease duration, degree of hypertension, sodium intake, and aldosterone exposure, and emerging modulators including oxidative stress, inflammatory biomarkers, endothelial dysfunction, genetic variants such as KCNJ5 mutations, and cortisol co-secretion [19,28,37,95]. The gene discussed is KCNJ5; the disease is cardiomyopathy.