AKT1 and neoplasm: Achievement of a motile and invasive phenotype by these tumor cells is supported by the abundant FSH bioavailability in post-menopausal age, which deregulates the E-cadherin expression as well as the molecular signaling driven by transforming growth factor β (TGF-β), Wnt/β-catenin, NOTCH, and PI3K/Akt pathways, resulting in typical cancer events, such as the disruption of epithelial integrity, loss of cell–cell junctions and, ultimately, the dissemination of tumor cells in blood [22].