AKT1 and neoplasm: EMT inducers such as TNF-alpha signaling through both the canonical Smad and non-Smad (Akt and ERK1/2), Wnt and focal adhesion pathways [9] activate oncogenic TFs and miRNAs whose gene expression regulation cause the enhancement of cell migration and epithelial scattering characteristic of EMT [8]; and this drives a subset of transformed primary epithelioid cells into self-renewing tumor-initiating cells or CSCs, (CD44hiCD24low) that efficiently generate new tumors due to clonal expansion, motility and invasive state that enable them to initiate local invasion and distal metastasis [7,9].