AGT is the sole precursor of RAS, synthesized by the liver, released into the circulation, and produces all active components of RAS.[11] To date, studies have demonstrated that among components of the RAS, plasma AGT levels exhibit a significant and independent correlation with cardiac diastolic function.[24, 25] This association persists even after adjusting for AngII‐dependent factors such as blood pressure and myocardial hypertrophy, suggesting that AGT may regulate diastolic function through AngII‐independent mechanisms. The gene discussed is AGT; the disease is cardiac hypertrophy.