Strikingly, the effects of MCT8/SLC16A2 mutations, which in human cause severe brain hypothyroidism with concomitant hyperthyroidism in circulation and peripheral organs, known as Allan-Herndon-Dudley syndrome (AHDS), characterized by severe intellectual and motor disability (257–259), are not fully recapitulated by mice, especially with regard to the neurological phenotype (91, 260–262). Here, SLC16A2 is linked to Allan-Herndon-Dudley syndrome.