TNFRSF11A and breast cancer: Accordingly, administration of medroxyprogesterone acetate (MPA) progestin was able to induce RANKL expression in mammary epithelial cells, whereas RANK genetic inactivation was able to abrogate MPA-induced epithelial proliferation and stem cell expansion, with a significant decrease in the incidence of MPA-driven mammary cancer, which onset was delayed [7].