Previous studies from our group also found that the blood adrenocorticotropic hormone (ACTH) and corticosterone levels in IUGR rats induced by PEE were lower after birth than those of the control rats [41, 64]; it was further confirmed that fetal rats exposed to alcohol during pregnancy had low adrenal function, mainly manifested by reduced expression of steroidogenic acute regulatory protein (StAR) and cytochrome P450 family 11 subfamily A member 1 (P450scc) [35, 37], suggesting that the low basal activity of the HPA axis caused by PEE originated from the fetus. Here, STAR is linked to fetal growth restriction.