In addition, analysis of the impact of IUGR on other interneuron (e.g., parvalbumin, vasoactive intestinal polypeptide, reelin) and cortical pyramidal cell (e.g., Cux1, SatB2, NECAB1) populations may provide further evidence to help support the proposal that an excitatory/inhibitory imbalance in the fetal IUGR brain contributes to behavioral deficits that manifest later in life. The gene discussed is RELN; the disease is fetal growth restriction.