A mutation in the gene for MCT8 (SLC16A2) results in the impairment of T3 uptake in the neurons, leading to the neurological deficit known as Allan–Herndon–Dudley syndrome (AHDS), an X-linked disorder, characterized by hypotonia, spasticity, muscle weakness, neurological disorders, and cognitive impairment [33,34,35]. This evidence concerns the gene SLC16A2 and Allan-Herndon-Dudley syndrome.