As the psychomotor retardation is thought to be caused by impaired neuronal triiodothyronine uptake during brain development, pharmacological efforts have concentrated on triiodothyronine analogues that do not require MCT8 for neuronal uptake.24 A recent pilot study with diiodothyropropionic acid,30 a thyroid hormone analogue that does not rely on MCT8 for tissue entry, resulted in normalization of laboratory thyroid parameters and reversed signs of peripheral hyperthyroidism but did not improve neurological features. The gene discussed is SLC16A2; the disease is hyperthyroidism.