GIST-T1 heterozygously expresses a Kit exon11 mutant Kit(Δ560–578), whereas GIST882 homozygously expresses Kit(K642E) (Supplementary Figure S2a).20, 36 GIST-R8 was established from GIST-T1 by continuous imatinib treatment, and this endogenously expresses Kit(Δ560–578/D820V) that confers imatinib resistance37 (Supplementary Figure S2a, bottom). This evidence concerns the gene KIT and gastrointestinal stromal tumor.