These findings contrast with the increasing number of non-genetic observational studies that point towards the pleiotropic effects of thyroid function (within the normal or subclinical range) on a wide variety of endpoints.1, 2, 3, 4, 5 Possible explanations include reverse causation, by which subclinical forms of diseases raise thyroid hormone levels, or missing or imperfect adjustment for common confounders. This evidence concerns the gene TG and thyroid gland disorder.