For example, human males with MCT8 mutations present with mental retardation (IQ <40), speech deficits and severe neurological abnormalities (known as the Allan-Herndon-Dudley syndrome), whereas MCT8 null mice are without an overt neurological phenotype (Kersseboom and Visser, 2011). Here, SLC16A2 is linked to Allan-Herndon-Dudley syndrome.