That is to say, PI3K-produced phospholipids favor the membrane recruitment of AKT which is further self-activated by either 3-phospho-inositidedependent protein kinase 1 (PDK1) or the mechanistic target of rapamycin (mTOR) complex 2 (mTORC2) [7, 39] it was reported that p-AKT signaling was much more activated in breast cancer cells and targeting PI3K/AKT signaling may be considered a prime strategy in cancer treatment [40]. Here, AKT1 is linked to breast carcinoma.