The cardiac-specific overexpression of METTL3 in mice has a protective effect on pathological myocardial hypertrophy, while cardiac-specific METTL3 knockout mice have been shown to exhibit abnormal cardiac function with aging and stress, indicating that a certain amount of RNA m6A is necessary to maintain cardiac homeostasis9,40. The gene discussed is METTL3; the disease is cardiac hypertrophy.