Although expression of EGFR was not associated with the malignant GIST phenotype [38] and was more likely to be an indicator of favorable prognosis in gastric GIST [39], combined targeting of EGFR and KIT increased efficiency of the treatment and abrogated resistance to tyrosine kinase inhibitor imatinib [40], revealing the importance and potential of EGFR as a therapeutic target. The gene discussed is KIT; the disease is gastrointestinal stromal tumor.