Moreover, we uncovered that RANKL silencing in Ishikawa could inhibit cell growth and promote cell apoptosis as well (Supplementary Fig. 5A) and overexpression of RANKL in T47D could enhance MPA-induced cell proliferation and decrease cell apoptosis (Supplementary Fig. 5B), thus further emphasizing the essential role of RANKL in the selective regulation of progesterone in EC and BC cells. This evidence concerns the gene TNFSF11 and breast cancer.