The pathogenesis of GIST is gain-of-function mutations of the proto-oncogene KIT in the majority, or platelet-derived growth factor receptor α (PDGFRA), with resultant encoding of related proteins, KIT, or PDGFRA receptors that contain ligand-independent kinase activity, leading to persistent and uncontrolled cell proliferation as well as resistance to apoptosis[1,2]. This evidence concerns the gene KIT and gastrointestinal stromal tumor.