The knockdown of methyltransferase-like 3 (METTL3) has also been shown to reduce m6A-mediated pri-miR-143 maturation into miR-143-3p, thus promotes cardiac regeneration after MI through miR-143-YAP/CTNND1 (catenin delta-1) axis [57]; whereas forced expression of m6A demethylase ALKBH5 also promotes cardiac regeneration after MI in mice and CM proliferation in hiPSC-CM by improving the mRNA stability of YTH N6-methyladenosine RNA-binding protein 1 (YTHDF1) and consequently promoting the translation of YAP [64]. This evidence concerns the gene YAP1 and myocardial infarction.