Progestin functions correlated to the presence of mPRs and mPR-dependent signaling in mammalian cells have been suggested to mediate the development of breast and ovarian hormone-sensitive cancers [137,138] since P4 has been observed to inhibit the EMT process in breast cancer cells through mPRs-mediated PI3K and EGFR activation [139] and to transduce through mPRs in ovarian cancer cells [140]. The gene discussed is EGFR; the disease is breast carcinoma.