All three Akt isoforms (Akt1, Akt2 and Akt3) were found to be overexpressed in human cancers [9,10,11,12,13,14,15,16,17,18,19], where, besides promoting tumor progression, they are also involved in conferring acquired resistance to many conventional chemotherapeutic agents [20,21,22], mainly for their contribution to the Epithelial-Mesenchymal Transition (EMT) occurring in drug-resistant and metastatic cancer cells [23,24,25]. This evidence concerns the gene AKT1 and neoplasm.