Indeed, Mct8/Dio2 KO and Mct8/Oatp1c1 KO mice replicate both the endocrine and neurological alterations present in patients, thus have been extensively used as a model of AHDS.24,26 Systemic administration of sobetirome and Sob-AM2 to Mct8/Dio2 KO mice was able to access the brain in the absence of MCT8 and modulate the expression of TH-target genes in juvenile mice.18 Because the neurological alterations in AHDS patients are already present from fetal stages,27 patients would benefit from prenatal treatment to prevent these defects. This evidence concerns the gene SLC16A2 and Allan-Herndon-Dudley syndrome.