KIT and gastrointestinal stromal tumor: Regorafenib had only modest activity against the KIT exon 13 V654A secondary mutation, which modifies a residue in the ATP-binding pocket of the kinase and is the most common secondary imatinib-resistance mutation in GIST patients following primary treatment with imatinib.18 In the present study, a patient progressed twice on a standard regorafenib dose/schedule, and on each occasion the regorafenib-resistance resulted from KIT V654A secondary mutation.