GIST usually develops from oncogenic mutations in the tyrosine kinase receptor KIT (CD117) [8], and/or platelet-derived growth factor receptor-α (PDGFR-α) [9]; the identification of c-KIT and PDGFR-α has resulted in the establishment of new therapeutic approaches based on therapies targeting the receptors, namely, MTT. This evidence concerns the gene PDGFRA and gastrointestinal stromal tumor.