Javidi-Sharifi et al. [77] suggest that some patients with gastrointestinal stromal tumor (GIST) treated with imatinib can develop a functional dependence on FGFR3, illustrated by the fact that the addition of the FGFR3 ligand FGF2 to GIST cells restored KIT phosphorylation during imatinib treatment. The gene discussed is KIT; the disease is gastrointestinal stromal tumor.