This was in agreement with our data illustrating that, in the presence of anti-FGF2 monoclonal Abs, KIT-inhibited GIST cells failed to produce VEGF-A and activate the VEGFR signaling cascade (Figure 1), thereby highlighting the pivotal regulatory role of the FGFR pathway in VEGFR signaling in GIST T-1R cells. The gene discussed is KIT; the disease is gastrointestinal stromal tumor.