When the factors inducing myocardial hypertrophy appeared, the expression of METTL3 mediated m6A methylation increases significantly, which promotes the occurrence of compensatory myocardial hypertrophy; when m6A methylation expression mediated by METTL3 is reduced and the observation time is long enough, it can lead to eccentric cardiomyocyte remodeling and cardiac dysfunction (62). This evidence concerns the gene METTL3 and cardiac hypertrophy.