Joshi et al. found that the expression levels of DNMT3A and DNMT3B were significantly reduced in the blood of patients under the age of 21 with several forms of congenital heart disease, such as ventricular or atrial septal defects and pulmonary stenosis, suggesting that decreased DNMT3 activity and the related genome’s hypomethylation may contribute to the pathogenesis of CHDs [144]. This evidence concerns the gene DNMT3B and atrial septal defect.