Data collected in patients with PRL excess due to a PRL-secreting pituitary tumour have evidently demonstrated that hyperprolactinemia is associated with an impaired gluco-insulinemic and lipid profile [21–38], accountable for the development of overt metabolic syndrome in approximately half of patients [33], irrespectively of concomitant hypogonadism [39], thus supporting the hypothesis that PRL excess may trigger an increased cardiovascular risk [40, 41]. The gene discussed is PRL; the disease is metabolic syndrome.