Indeed, our data in the heterozygous KIT mutant GIST-T1 cells indicate that autocrine/paracrine KITLG-mediated KIT signaling may account for ~40% of baseline proliferation even in cells with a secondary, imatinib-resistant mutation and can be inhibited with antibodies or RNAi targeting KITLG. Here, KIT is linked to gastrointestinal stromal tumor.