As both the ligand and receptor for stromal FGF signalling were increased in the bevacizumab-treated tumours, we focused on stromal FGF2 as a candidate molecule for the acquired resistance to anti-VEGF therapy, and confirmed that the protein expression of mouse FGF2 was significantly increased in the pleural effusion of bevacizumab-treated Y-MESO-14 tumour-bearing mice (Fig. 2b). This evidence concerns the gene VEGFA and neoplasm.