 It has been suggested that "DLX" promotes the migration of interneurons by repressing a set of proteins that are normally expressed in terminally differentiated neurons and act to promote the outgrowth of dendrites and axons.Mice lacking DLX1 exhibit electrophysiological and histological evidence consistent with delayed-onset epilepsy.DLX2 has been associated with a number of areas including development of the zona limitans intrathalamica and the prethalamus.