These tissue-specific effects argue against a general alteration in MCT8 activity being part of the etiology of IUGR, but rather suggest that altered cerebral MCT8 expression is a local adaptive response to the growth-restricted state that is associated with chronic distress, which is supported by our finding that the greater the growth restriction, the lower the MCT8 expression. The gene discussed is SLC16A2; the disease is fetal growth restriction.