Hypopituitarism or a direct action of GH and IGF-I excess on the pituitary–gonadal axis or the co-existence of hyperprolactinemia due to mass effect or to prolactin hypersecretion by the tumor have been proposed as potential mechanisms for the impairment in gonadotropin secretion, leading to ovarian dysfunction and consequent infertility [108–110]. This evidence concerns the gene GH1 and neoplasm.