Placental SNAT2 has been reported to be highly regulated by a variety of environmental factors including in vitro culture conditions [7], hormones (glucocorticoid exposure) [24,38,39], pH, oxygen tension [40], high fat diet [41], maternal protein restriction [42] and in obstetric conditions such as intrauterine growth restriction (IUGR) [43,44]. Here, SLC38A2 is linked to fetal growth restriction.