Both of these research paths have identified many AR mechanisms to first- and second-generation EGFR-TKIs, including T790M EGFR secondary mutation, as the most common mechanism, followed by MET gene amplification, ERBB2 gene amplification, small-cell lung cancer (SCLC) transformation, and the acquisition of epithelial to mesenchymal transition (EMT) features [13]. The gene discussed is EGFR; the disease is small cell lung carcinoma.