Despite the proven biochemical and tumoral efficacy of DAs in prolactinomas, a minority of patients, accounting for 10% of patients with macroprolactinoma and less than 20% of those with macroprolactinoma (24, 25), fail to achieve the biochemical control of PRL excess and/or the reduction in tumor mass during treatment with DAs (6, 26). The gene discussed is PRL; the disease is neoplasm.