Thyroid hormone (T3) plays important roles during vertebrate development (1 ). In humans, T3 is detected in the embryonic plasma by 6 mo and rises to high levels around birth (2 ). During this postembryonic period, extensive tissue remodeling and organogenesis take place. T3 deficiency during human development leads to developmental defects, such as mental retardation, short stature, and in the most severe form, cretinism (1 ,3 ). Likewise, T3 is also critical for amphibian development. It is the controlling agent of anuran metamorphosis, a process that transforms a tadpole into a tailless frog (1 ,4 ). Blocking synthesis of endogenous T3 leads to the formation of giant tadpoles that cannot metamorphose, while addition of exogenous T3 to premetamorphic tadpoles causes precocious metamorphosis. Importantly, most, if not all, organs are genetically predetermined to undergo specific changes, and these changes are organ autonomous. Thus, T3 appears to act directly on individual metamorphosing organs. Such properties have made anuran metamorphosis one of the best-studied postembryonic developmental process at morphological, cellular, and biochemical levels and paved the way for current molecular investigations of the underlying mechanisms.