Data presented in this report show that FGF-2-expressing tumors represent a subset of tumors characterized by Akt3 overexpression, alternative splicing of FGFR-2 toward the IIIc splice variant, which facilitates the response to FGF-2,6 and activation of the FGF-2/KDM2B-EZH2/miR-101/EZH2 pathway.11,12 FGF-2-expressing tumors also tend to express high levels of CTLA-4, PD-1 and PD-L1, which suggests immune checkpoint activation as a mechanism for the blockade of the host immune response against the tumor. This evidence concerns the gene AKT3 and neoplasm.