To gain greater insight into the pathophysiology of AHDS, researchers have looked into the brains of animal models expressing a nonfunctional MCT8 and studied neural cells derived from induced pluripotent stem cells (iPSCs) and found that MCT8 plays a role in the passage of TH through the blood-brain barrier (11–13). The gene discussed is SLC16A2; the disease is Allan-Herndon-Dudley syndrome.