Evidence supporting this notion are: First, recurrent tumor samples from all 8 IMA-resistance-GIST patients showed significantly increased KIT protein expression, even in the two patients with secondary mutations detected in their KIT gene; Secondly, down-regulation of KIT re-sensitized IMA-resistance-GISTs to Imatinib; Thirdly, KIT up-regulation likely increased overall KIT tyrosine kinase activity and stimulated growth of GISTs in the presence of Imatinib. Here, KIT is linked to gastrointestinal stromal tumor.