In instances of SLC16A2 mutation, the dysfunction of MCT8 results in insufficient intracellular levels of T3 in the presence of increased serum free levels, which results in hypomyelination and the severe psychomotor retardation seen in Allan-Herndon-Dudley syndrome (AHDS) (Friesema et al., 2004; Armour et al., 2015; Valcárcel-Hernández et al., 2022). The gene discussed is SLC16A2; the disease is Allan-Herndon-Dudley syndrome.