KIT and gastrointestinal stromal tumor: Specifically, GIST cells in which KIT exon 11 primary mutation was coupled to a secondary mutation in exon 13 V654A mutation were inhibited only by sunitinib, whereas GIST cells with KIT exon 11 primary mutation coupled to an exon 14 T670I gatekeeper mutation were inhibited by sunitinib and regorafenib (Fig. 1b), and GIST cells with KIT exon 11 primary mutation coupled to exon 17 D816E or D820A or exon 18 A829P activation loop mutations were inhibited by regorafenib only (Fig. 1c).