Conditions known to interfere with normal neurodevelopment by compromising TH action include iodine deficiency, maternal and fetal hypothyroidism or hypothyroxinemia, and mutations of the nuclear TH receptor (TR) alpha and beta as well as of monocarboxylate 8 transporter (MCT8) gene SLC16A2 [9]. This evidence concerns the gene SLC16A2 and hypothyroidism.