NKX2-1 and congenital hypothyroidism: The observed synchronized induction of GLIS3 and NIS protein expression during embryonic development, the suppression of Slc5a5 expression in GLIS3-deficient thyroids, and the observation that GLIS3 is expressed at E15.5, much later than PAX8 and NKX2.1 [4, 8, 50], are consistent with the hypothesis that in GLIS3-deficient mice the development of congenital hypothyroidism is due to dyshormonogenesis rather than thyroid dysgenesis [33].