These findings led to the conclusion that PRL acts via an autocrine or paracrine mechanism to modulate growth of uterine smooth muscle cells in a dose-dependent manner: cell growth and proliferation was promoted at low PRL concentrations and inhibited at high PRL concentrations, suggesting a potential role for PRL in the pathogenesis of leiomyomas (41) and raising the question of whether PRL suppression by medical treatment with dopamine agonists might impact clinical outcome of patients with uterine leiomyomas. This evidence concerns the gene PRL and uterine corpus leiomyoma.