The mammalian target of rapamycin (mTOR) pathway, which is likely to play a central role, can be stimulated or inhibited directly or indirectly by circulating macronutrients, cortisol, adiponectin, IGF1, leptin or insulin, or by changes in uteroplacental blood flow [42], which may explain how placental insufficiency can develop despite normal nutrient availability. Here, LEP is linked to placental insufficiency.