FGF2 and neoplasm: Interestingly, BGJ398, the FGFR kinase inhibitor, induced a significant (~6-fold) increase of FGF-2 levels in supernatants of IM-treated GIST-T1R cells on day 2 post-treatment (Figure 1G) and this fact correlated with an increase of mRNA FGF-2 (Figure 1F), thereby indicating the possibility of the decreased consumption of FGF-2 produced by tumor cells after the inhibition of the FGFR-signaling pathway.