Although the pathophysiology behind fetal hypoxia in hyperglycemic pregnancies has been examined mainly in animal studies and in type 1 diabetes in humans, [23–25] elevated markers of fetal hypoxia, such as abnormal cord blood acid–base status and increased cord EPO levels at birth, occur also in GDM pregnancies, [25, 26] suggesting the same underlying pathogenesis. This evidence concerns the gene EPO and gestational diabetes.