Using whole-exome sequencing of several multi-generational pedigrees of German descent with high density of ADHD we identified a triplet ATG deletion in SLC5A4 leading to a loss of the amino acid methionine in the 11th transmembrane segment (TM11) in hSGLT3 (ΔM500) co-segregating—although imperfectly—with the clinical phenotype of ADHD. This evidence concerns the gene SLC5A4 and attention deficit-hyperactivity disorder.