MAPK1 and breast carcinoma: However, unlike in breast cancer cells, P4-triggered mPR activity has been shown to indirectly induce cAMP levels by enhancing β1,2-adrenergic receptor activation and to up-regulate apoptosis regulator BAX (also known as Bcl-2-like protein 4) through JNK1/2 and p38 MAPKs activation [148], indicating the existence of mPR-induced molecular pathway that, through pro-apoptotic MAPK signaling modules, can lead to ovarian cancer cell death and suggesting that P4-based hormone therapy could provide a suitable and effective strategy for the treatment of ovarian cancer [148] (Figure 3).