AHDS-like symptoms could be replicated only by simultaneous inactivation of MCT8 and another TH transporter, OATP1C1, in mice (Mayerl et al., 2014), from which we presumed that impaired TH transport across the BBB and/or BCSFB is the major abnormality driving the disease phenotype. Here, SLCO1C1 is linked to Allan-Herndon-Dudley syndrome.