The exact mechanism by which maternal hyperglycemia affects fetal cardiac morphology and function is still unknown, prior research has shown that the various mechanisms share many pathogenic pathways, including metabolic disturbance and hyperinsulinemia, dysregulation of the insulin-like growth factors [32, 35], oxidative stress [36], and inflammatory pathways [32], changes in loading conditions and fetal hypoxemia, which cause cardiomyocyte injury and apoptosis, resulting in myocardial deformation and dysfunction [7, 8, 12, 32, 33, 37], which are yet to be defined completely. The gene discussed is INS; the disease is hyperinsulinism.