FTO is highly expressed in fetal heart ventricles and has been demonstrated by numerous studies to be closely involved in the pathogenesis of congenital heart disease [including hypertrophic cardiomyopathy (HCM), atrial septal defect (ASD) and ventricular septal defect (VSD)] (130), arrhythmias (131), coronary artery disease (CAD) (132), and metabolism-related heart disease (including obesity and type 2 diabetes) (133, 134). Here, FTO is linked to obesity due to melanocortin 4 receptor deficiency.