These mechanisms have been demonstrated in allograft transplantation experiments and in mouse model of pancreatic NEN (the Rip1Tag2 transgenic mice), where interfering with the FGF function by a soluble form of the FGFR2 IIIb significantly inhibited tumor-induced angiogenesis and tumor growth (64). This evidence concerns the gene FGFR2 and pancreatic neuroendocrine neoplasm.