Partial hypogonadism occurs in about 1/3 of patients; it is mainly identified through menstrual irregularities in females and through central hypogonadism, delayed sexual development, and decreased libido in males.[6] In our case, the laboratory findings indicated increased TSH, free T3, free T4, hypopituitarism (pituitary-adrenal axis, pituitary-gonad axis, and growth hormone defects), and visual confirmation of an adenoma-like mass through MRI, which are consistent with a TSH-producing adenoma, though the typical clinical signs of hyperthyroidism were absent. This evidence concerns the gene GH1 and hypogonadotropic hypogonadism.