Examples include mutations in the glycine transporter-2 (GlyT2/SLCA5) that give rise to hypereplexia/startle disease (3), in the creatine transporter-1 (CRT1/SCL6A8) that account for ∼5% of male mental retardation (4), and in the dopamine transporter (DAT/SLC6A3)5 that lead to a syndrome of infantile/juvenile dystonia or dopamine transporter deficiency syndrome (5, –, 7). Here, SLC6A5 is linked to hereditary hyperekplexia.