Interestingly, FGFR3 silencing restored imatinib response in imatinib-resistant GIST cells, whereas the addition of FGF2 to GIST cells induced KIT signaling, increased cell proliferation and desensitized GIST cells to imatinib, suggesting the existence of a crosstalk between the two receptors. The gene discussed is KIT; the disease is gastrointestinal stromal tumor.