Our data illustrates that FGF-2 is actively secreted by IM-treated and KIT-inhibited GISTs (Figure 1D), activates FGF-signaling via phosphorylation of FGFR1 and -2 (Figure 3) and translocates into the nucleus (Figure 6D and Figure 7A), thereby illustrating the variety of FGF-dependent mechanisms of GIST resistance to IM-induced apoptosis. The gene discussed is FGFR1; the disease is gastrointestinal stromal tumor.