Through mechanisms linked to chronic systemic hyperglycemia, local inflammation and the release of pro-inflammatory and pro-angiogenic molecules such as vascular endothelial growth factor (VEGF), advanced glycation end-products (AGE) and alterations to de novo synthesis of nitric oxide (NO), maternal hyperglycemia is known to induce vascular defects characterized by increased angiogenesis, increased vascular resistance, hyper-coagulability and preponderance of highly permeable vessels [55–59]. This evidence concerns the gene VEGFA and Hyperglycemia.