Subsequently Shen et al. [37] demonstrated that mTORC2 activity is selectively upregulated in endometrial cancers, as evidenced by the overexpression of nuclear p-mTOR and p-Akt, as well as by the overexpression of VEGF-A isoform and PLD1 in malignant epithelium. This evidence concerns the gene AKT1 and endometrial cancer.