According to our previous studies, the expression of RANKL was upregulated in EC tissues and administration of medroxyprogesterone acetate (MPA) was able to inhibit the EC cell behavior induced by RANKL via progesterone receptor (PR) [20], while in BC, treatment with MPA triggered massive induction of RANKL in luminal epithelial cells, leading to increased proliferation of mammary epithelial cells, thus giving rise to mammary tumor in combination with a chemical carcinogen, 7,12-dimethylbenz[a]anthracene (DMBA) in vivo [21]. This evidence concerns the gene PGR and breast cancer.