Currently, MCT8-deficient patients have limited treatment options and, because of the clinical complexity of the syndrome, with both cerebral hypothyroidism and peripheral hyperthyroidism, the designing of therapeutic strategies is challenging.7 Among those strategies that have been clinically tested, both TH replacement strategies, such as the combination of PTU and levothyroxine, and TH analog strategies, including diiodothyropropionic acid and triiodothyroacetic acid (TRIAC), have been able to ameliorate key features related to peripheral hyperthyroidism. This evidence concerns the gene SLC16A2 and hyperthyroidism.