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. The gene discussed is PDGFRA; the disease is gastrointestinal stromal tumor.