SLC16A2 and Allan-Herndon-Dudley syndrome: Mice with a concomitant inactivation of Mct8 and the T4-specific transporter Oatp1c1 (Mct8/Oatp1c1 knockout (DKO) mice) replicate the peripheral endocrine abnormalities of MCT8 patients and show a profound TH-deficient status in the CNS, thus representing an established animal model of AHDS [6].