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. Here, IGF1 is linked to fetal growth restriction.