Similarly, FGFR inhibitor indicated above substantially attenuated the phosphorylation of both forms of FRS-2 in IM-naive GIST T-1 cells treated by FGF-2 (Figure 4E), thus confirming a high potency of BGJ398 to inhibit FGF-signaling pathway activated via the autocrine (e.g., by FGF-2 secreted from IM-resistant GISTs) or paracrine (e.g., activated by exogenous FGF-2) mechanisms. Here, FRS2 is linked to gastrointestinal stromal tumor.