Han et al. (2021) reported that ALKBH5-mediated m6A regulates cardiomyocyte proliferation and regeneration by improving the stability of YTHDF1 and promoting the translation of YAP. Next-generation sequencing results uncovered that m6A landscape is altered in heart failure and heart hypertrophy, and leads to protein abundance changes independent of mRNA levels (Berulava et al., 2020). These findings enhance our understanding that the relationship between m6A modification and origin of cardiovascular disease. Here, YTHDF1 is linked to cardiovascular disorder.