Rather, the primary mechanism behind the thyroid phenotype previously observed in offspring seems to be in the thyroid gland, in which lower responsivity to TSH requires higher circulating TSH levels to produce adequate quantities of thyroid hormones, a condition resembling early autoimmune thyroid failure, leading to subclinical hypothyroidism, characterized by normal serum T4 and high normal serum TSH concentrations. This evidence concerns the gene TG and thyroid gland disorder.