The pathogenesis of hyperprolactinemia in hypothyroidism remains unclear; the mainstream hypothesis is that TRH can not only activate the TSH-secreting cells but also stimulate the PRL-secreting cells, and the enlarged pituitary gland compresses the pituitary stalk affecting the hypophysioportal circulation and resulting in reduced dopamine (an antagonist against the PRL releasing hormone). The gene discussed is PRL; the disease is hypothyroidism.