Neurological deficits caused by fetal exposure to ethanol remains prevalent and are recognized as a serious public health issue. The effects of fetal alcohol exposure are multifaceted and is characterized by multiple structural malformations and cognitive deficiencies, however the basic molecular mechanisms central to these defects are not thoroughly understood. A central factor in embryonic development is posttranscriptional gene regulation. Post-transcriptional regulation governs all aspects of development and is an area of vulnerability that is targeted by ethanol. nELAVs RNA binding proteins are important post transcriptional regulators involved in RNA translocation and stability. Elucidating ethanol's effects as a teratogen on these regulators their target transcripts and binding partners will enable us to implement strategies to diminish several long-term effects of fetal ethanol exposure.