It has been widely well-recognized that aberrant AKT activity is the central hub of numerous signaling pathways driven by activation of oncogenes or loss of tumor suppressors, such as EGFR and other receptor tyrosine kinases, Ras, PI3K, BRAF, AKT itself, and natural AKT inhibitor PTEN, and plays pivotal role during tumor development and progression30,31. This evidence concerns the gene AKT1 and neoplasm.