Ultimately, responses and possibly prolonged survival were reported with the off-label use KIT inhibitors—imatinib, sunitinib, or sorafenib—in patients with KIT-mutant thymic carcinoma, mostly in single-case observations21; phase II trials with sunitinib also identified such mutations among some long-term responders, but response observed in those studies was mostly attributed to the angioangiogenic effect through inhibition of vascular endothelial growth factor receptors.22,23 A second pathway of clinical relevance in thymic epithelial tumors is the PI3K pathway. The gene discussed is KIT; the disease is thymic carcinoma.