Therefore, in pathological situations of either maternal or fetal thyroid hormone deficiency during pregnancy, certain transporters could compensate for a lack of TH in placenta, such as a compensatory up-regulation of MCT8 in placentae from IUGR pregnancies delivered in the early 3rd trimester compared to age matched appropriately grown for gestational age controls [20], [21]. Here, SLC16A2 is linked to fetal growth restriction.