The wild-type GIST, nearly 10 % of GISTs and poor responders to imatinib, may have various genomic or epigenetic alterations in succinate dehydrogenase (SDH), neurofibromatosis type 1 (NF1), BRAF, or RAS. Molecular matching is suggested to be effective in SDH-deficient GISTs [38–40] and NF1-GISTs [41]. Here, BRAF is linked to gastrointestinal stromal tumor.