KIT protein overexpression was observed in the majority of GIST cases, while gain-of-function mutations in the KIT gene lead to activation of downstream signaling pathways, including MAPK, PI3K-AKT-mTOR, JAK-STAT and result in promoted tumor growth and inhibition of apoptosis [22,23,24,25], making KIT an attractive target for cancer therapy. This evidence concerns the gene SOAT1 and gastrointestinal stromal tumor.