In these oncosomes,KIT is constitutively activated, which triggers the phenotypic conversionof progenitor smooth muscle cells to tumor-promoting cells. Furthermore, the researchers could use theseoncosomes and associated exosome proteins, discovered through thefirst high-quality proteomic study of GIST-derived exosomes, to trackdisease burden in patients receiving imatinib mesylate. This evidence concerns the gene KIT and gastrointestinal stromal tumor.