Indeed, with the identification of activating mutations of either KIT or platelet-derived growth factor receptor (PDGFRA) tyrosine kinases as main players in GIST pathogenesis and development, in few years, imatinib has become the backbone for the treatment of unresectable and advanced GIST, whose efficacy is profoundly affected by the underlying tumor genotype [2,3,4,5]. This evidence concerns the gene KIT and gastrointestinal stromal tumor.