Phase II and III imatinib trials in patients with advanced GIST reported higher partial response rates and longer overall survival in patients with mutations in KIT exon 11 compared to patients with a mutation in KIT exon 9 or no detectable mutations (GIST wild-type) [12] Furthermore, almost all patients who experience early disease progression on imatinib treatment (400 mg/day) have mutations in KIT exon 9 or in PDGFRA, or are wild type for the known KIT and PDGFRA mutations [5]. Here, KIT is linked to gastrointestinal stromal tumor.