Moreover, the view of further MCT8 functions besides T3 transport would be compatible with observations made in patients with MCT8 loss-of-function mutations who are affected by Allan–Herndon–Dudley Syndrome (AHDS), a severe developmental disease that is argued to be caused by the lack of T3 transport due to the disturbed transport function of MCT8 itself [56]. The gene discussed is SLC16A2; the disease is Allan-Herndon-Dudley syndrome.