Although the underlying physiological mechanisms are insufficiently understood, these conditions might share fundamental pathophysiological processes: a sequence variant predicting E219D, found in some individuals with Tourette syndrome (Adamczyk et al., 2011), increases the relative probability of surface membrane insertion for human EAAT1 and SLC1A3 duplication is likely to increase EAAT1 expression in attention-deficit hyperactivity disorder and autism. This evidence concerns the gene SLC1A3 and attention deficit-hyperactivity disorder.