EGFR-TKIs, including erlotinib and gefitinib, can induce plasma membrane-associated EGFR protein degradation[16], and the inhibition of STAT3 abrogates erlotinib resistance in lung cancer cells[28], suggesting that a high level of plasma membrane-associated EGFR may be important in EGFR-TKI resistance. The gene discussed is STAT3; the disease is lung cancer.