Therefore, we generated mice with cardiomyocyte-specific deletion of Dnmt3a and Dnmt3b. To gain insight into the relevance of de novo CpG methylation in cardiac hypertrophy and failure, we subjected these mice to left ventricular pressure overload by transverse aortic constriction and analysed cardiac gene expression and DNA methylation. This evidence concerns the gene DNMT3A and cardiac hypertrophy.