We in fact demonstrated that Stat3 acts as a PR co-activator at the promoters of the mouse mammary tumor virus (MMTV) and the endogenous gene bcl-X in breast cancer cells [71], raising the possibility that the role of Stat3 as a PR co-activator is a general mechanism for the modulation of the transcriptional effects of PR. This evidence concerns the gene STAT3 and breast carcinoma.