Many factors including mechanical stress and neurohumoural stimulation induce cardiac hypertrophy.1 Among them, angiotensin II (AngII), a degraded peptide from the renin‐angiotensin system, is one of the most powerful stimuli in inducing cardiac hypertrophy and fibrosis.2 In patients with an excessive activated RAS (rennin‐angiotensin system) or enhanced responsiveness to AngII, the inappropriate remodelling and vascular diseases were initiated.3 The gene discussed is REN; the disease is cardiac hypertrophy.