The PI3K/AKT/mTOR signaling pathway is strongly involved in the fundamental cellular processes of protein synthesis and apoptosis, and disturbed activation of this intracellular pathway has been associated with the development of diseases such as cancer, diabetes mellitus, and autoimmunity[1]. Upon activation of  phosphatidylinositol (PI)-3-kinase (PI3K) by extracellular growth factors, phosphorylation of the inner membrane phosphoinositides activates AKT (also known as Protein Kinase B, PKB) and PDPK1 (3-phosphoinositide dependent protein kinase-1). In turn, mTOR (mammalian target of rapamycin)  is activated downstream, which plays an important role in cell cycle progression[2]. In many cancer cells, this PI3K/AKT/mTOR pathway is highly active, which can be the result of  amplification or mutation of the PI3-kinase gene; amplification or mutation of the Akt gene; or loss of function of PTEN (Phosphatase and tensin homolog). The latter normally regulates the removal of phosphate groups of the PI3K mediated phosphorylated membrane phospholipids, one of the regulating mechanisms to prevent over activations of this pathway.