In an earlier companion study, we demonstrated that experimental chronic gestational exposure to ethanol led to increased fetal loss, IUGR, placentation abnormalities, and fetal morphogenic attributes reminiscent of FASD.1 These ethanol-induced effects were associated with altered expression of insulin, IGF, and downstream signaling proteins and phospho-proteins.1 The shifts in phospho-protein levels correspond with the net dynamic results of kinase and phosphatase activities, along with the expression levels of corresponding signaling molecules. This evidence concerns the gene PROS1 and fetal growth restriction.