KIT and gastrointestinal stromal tumor: Expression of VEGF (a highly pro-angiogenic ligand of VEGFR2, which is another target of sunitinib but not of imatinib) has been shown to be higher in wild-type GISTs than in KIT-mutant GIST [38], and little is known about the angiogenic status at the time of progression on imatinib, which is likely to play a role in the mechanisms of resistance, as with many other targeted therapies.