Several mechanisms of acquired resistance to EGFR TKIs have been identified, including a second-site point mutation that substitutes methionine for threonine at position 790 (T790M) in the EGFR, amplification of the mesenchymal-epithelial transition (MET) proto-oncogene and human epidermal growth factor receptor 2 (HER2), and small-cell lung cancer transformation [8–10]. Here, EGFR is linked to small cell lung carcinoma.