It has been found that after knocking out the methyltransferase DNMT3b in the heart of adult mice, it was found that the myocardial contractility of mice was weakened, the myocardium became thinner, and the myocardial fibers and muscle nodules were disordered, which could lead to a decline in cardiac function and eventually heart failure, and the methylation levels of DNMT3b promoter and CpG island in myocardial tissue were significantly reduced compared with the normal control group [22]. Here, DNMT3B is linked to heart failure.