Moreover, the activation of different phosphorylated site of STAT3, such as S727 and Y705, may lead to different downstream effect.28 The JAK/STAT activation induced by angiotensin II is biphasic and time dependent in rat cardiomyocytes.29 Our findings revealed a detrimental role of STAT3 in the ischaemia‐related cardiac hypertrophy, which is not consistent with our previous report. The gene discussed is AGT; the disease is cardiac hypertrophy.