Compelling evidence suggests that aldosterone over-production is an important substrate for TRH.5,6 Excessive aldosterone may promote inflammation and fibrosis in myocardial, vascular, and renal tissues, thereby leading to the progression of TRH and CKD severity.7,8 While optimized blood pressure (BP) control is crucial for reducing cardiorenal risk, excessive aldosterone can increase the risk regardless of BP levels.9,10 Both achieving BP control and mitigating the risk of aldosterone-associated cardiorenal outcomes should be the focus when managing patients with TRH and CKD. The gene discussed is TRH; the disease is chronic kidney disease.