SLCO1C1 and Allan-Herndon-Dudley syndrome: 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.