Moreover, given that FGF-2 signals via the IIIc isoform of FGFR-2, which is normally expressed in mesenchymal cells and in invasive and metastatic tumors undergoing EMT,9,10 these findings also suggest that the EMT-promoting activity of FGF-2 is under the control of Akt3 which promotes the alternative splicing of FGFR-2 by phosphorylating IWS1. This evidence concerns the gene AKT3 and metastatic neoplasm.