Of note, treatment with the Akt inhibitor MK2206 upregulated PR expression in endometrial cancer cells and in one low-grade endometrial PDX model, but not in two other high-grade PDX models, highlighting the urgent need to identify better agents to induce PR in high grade tumors where resistance to progestin hormonal therapy is most common [19,20,39]. This evidence concerns the gene AKT1 and endometrial cancer.