The most common mutation is c-KIT exon 11, followed by c-KIT exon 9, while mutations in c-KIT exons 13, 14, 17, and 18 are rare.[17,18] In recent years, the application of tyrosine kinase inhibitors targeting c-KIT and PDGFRA genes, such as imatinib, has achieved a breakthrough in the treatment of GIST, with 83% to 89% of patients with advanced GIST benefiting from imatinib.[19,20] Given that the therapeutic effect of imatinib is directly related to the mutation status, it is necessary to conduct mutation analysis by immunohistochemistry before imatinib treatment. Here, KIT is linked to gastrointestinal stromal tumor.