Extra-pituitary Prl production in humans, due to the presence of a separate gene promoter, has been elegantly shown by Horseman et al. by replacing the mouse Prl promoter with its human counterpart [35,36].Taken together, there is room to hypothesize that LAM lesions are hypersensitive to endocrine or locally produced Prl, and that LAM lesions will respond to agents disrupting Prl signals. The gene discussed is PRL; the disease is lymphangioleiomyomatosis.