Collectively these data indicate that roughly one out of five patients diagnosed with a KIT/PDGFRA/SDH/RAS-P wild-type GIST is a bona-fide carrier of pathogenic KIT mutation, thus expected to be eligible for and responsive to the various therapeutic lines of TK-inhibitors approved for KIT/PDGFRA-mutant GIST. Here, TKT is linked to gastrointestinal stromal tumor.