Indeed, with the identification of activating mutations of either c-KIT or platelet-derived growth factor receptor (PDGFRA) tyrosine kinases as main players in GIST pathogenesis and development, in a few years, imatinib has become the backbone for the treatment of unresectable and advanced GISTs, the efficacy of which is profoundly affected by the underlying tumor genotype [6]. This evidence concerns the gene PDGFRA and neoplasm.