Based on the molecular pathogenesis of driver gain-of-function mutations in c-kit (80-90%) [1-4] and less frequently in the PDGFRα gene (5-10%), gastrointestinal stromal tumors (GIST) became a molecular model tumor in oncology emphasized by the central role of receptor tyrosine kinases in their molecular pathogenesis and the availability of small molecule inhibitor therapy. This evidence concerns the gene KIT and gastrointestinal stromal tumor.