Emerging evidence suggests that overexpression of METTL3 controls left ventricular shortening fraction and ejection fraction, upregulates the expression of hypertrophic markers, induces myocardial fibrosis, impairs cardiac function and reverses the anti-hypertrophic effects of hawthorn acid, ultimately leading to pathological cardiac hypertrophy [137]. Here, METTL3 is linked to Myocardial fibrosis.