MET, in a dose-dependent manner, exerted an inhibitory proliferative effect on ovarian tumor cells (HEY, CAOV-3, SW626), whereas the neutralization of MET promoted cell proliferation and the silencing of the opioid growth factor receptor favored tumor cell replication; MET, via the opioid growth factor receptor, delayed cells moving by upregulating the cyclin-dependent inhibitory kinase pathways [16,245]. This evidence concerns the gene MET and ovarian neoplasm.