By bioinformatic analysis, we were not only able to confirm and expand the list of proteins linked to deficits in myelination and neurogenesis, but also disclosed distinct alterations in signaling pathways and in the expression of specific molecules that have not been considered as targets of TH action in AHDS, but that in humans are linked to movement disorders and may thus be of relevance for patients with MCT8 deficiency. Here, SLC16A2 is linked to Allan-Herndon-Dudley syndrome.