Considering that placental mTORC1 activity and GLUT3 expression are decreased in intrauterine growth restriction and that placental GLUT3 mutation has been shown to cause late-gestational fetal growth restriction, we tested one of the possible mechanisms for the development of abnormal fetal growth in this pregnancy complication: the decrease of placental GLUT3 levels resulted from inhibition of mTORC1 signaling may be one important mechanism in fetal growth restriction. The gene discussed is SLC2A3; the disease is fetal growth restriction.