The oncogenic reliance of GISTs upon mutated KIT/PDGFRA is emphasized by their sensitivity to imatinib mesylate (IM), a tyrosine kinase inhibitor (TKI) that targets both KIT and PDGFRA kinase activity, leading to substantial tumor shrinkage with durable responses in most patients [6, 7]. Here, PDGFRA is linked to neoplasm.