KIT and gastrointestinal stromal tumor: The imatinib-resistance mechanisms responsible for clinical progression in KIT-mutant GISTs commonly involve emergence of polyclonal subpopulations with secondary KIT kinase domain mutations.8–11 KIT-independent mechanisms leading to imatinib-progression in KIT-mutant GIST have been reported but are infrequent and yet to be thoroughly studied.17,30 Therefore, KIT inhibitory strategies after failure of imatinib remain useful because most imatinib-resistant GISTs are still dependent upon KIT signalling for survival and proliferation.