In cancer, PI3K-Akt-mTOR is activated via multiple mechanisms, including phosphatase and tensin homolog (PTEN) mutation (PI3K-Akt signaling negative regulator) [1], [2], Akt overexpression [3], [4], and the activation of upstream signaling pathways (receptor tyrosine kinase and Ras) [5], [6] that are associated with cancer cell proliferation, tumor growth, metastasis, and cell survival [7]–[10]. Here, AKT1 is linked to neoplasm.