Viewed in the context of the results of our earlier studies, these data suggest that the tumor phenotype may be due to the promotion of FGF-2 responsiveness by the Akt3/IWS1 pathway and the induction of EMT and stem cell self-renewal by FGF-2 via the FGF-2/KDM2B/miR-101/EZH2 pathway. This evidence concerns the gene AKT3 and neoplasm.