In the zebrafish model, the developmental action of MTH through Mct8 can be examined without major compensatory mechanisms such as maternal TH compensation, endogenous TH production, or increased uptake by co-expressed TH transporters, as occurs in the mouse model (39), where a similar model of AHDS was only achieved after double KO of Mct8 and Oatp1c1 (40–42) or Mct8 and D2 (43). The gene discussed is SLC16A2; the disease is Allan-Herndon-Dudley syndrome.