Overexpression of METTL3 can induce compensatory cardiomyocyte hypertrophy without deteriorating cardiac function (Dorn et al., 2019), whereas knockout of METTL3 upregulates PARP10 expression via down-regulation of m6A methylation of Parp10 mRNA, and accelerates pathological cardiac hypertrophy (Gao et al., 2020; Table 3 and Figure 2). This evidence concerns the gene METTL3 and cardiac hypertrophy.