KIT and gastrointestinal stromal tumor: In vitro, sunitinib is more active on KIT GIST cell lines bearing secondary mutations at the ATP-binding pocket (exons 13 and 14) than in GIST cell lines harboring imatinib-resistant mutations at the activation loop (exons 17, mutations D820Y, D820E, and N822K, and exon 18 A829P) [109,120].