RES significantly alleviates cardiac oxidative injury induced by fenitrothion and repaired the transcript levels of SIRT1, c‐JNK, and caspase‐9/3, along with p53 immunoreactivity [103]. RES treatment significantly improves left ventricular function and reduces left ventricular hypertrophy and cardiac fibrosis in pressure overload rats by regulating the SIRT1/TGF‐β1/p‐Smad3 signaling pathway [104]. The gene discussed is SIRT1; the disease is left ventricular hypertrophy.