The role of mechanistic pathways other than those related to fetal hyperinsulinemia is supported by studies in non-diabetic conditions – such as fetal growth restriction, hypertensive disorders and post-term pregnancies – that are also characterized by increased risks of fetal hypoxia, high EPO and stillbirths (7, 22, 48) as well as later adverse metabolic health outcomes in the offspring (49–51). The gene discussed is EPO; the disease is Hyperinsulinemia.