Postmortem analysis performed on an 11-year-old AHDS boy has revealed prominent hypomyelination by MBP immunostaining [96], strongly suggesting that the availability of T3 within the CNS may be abrogated specifically in OLs due to the lack of functional MCT8, thereby limiting the differentiation capacity of this cell lineage, causing dysmyelination during brain development. This evidence concerns the gene SLC16A2 and Allan-Herndon-Dudley syndrome.