Mechanisms of resistance, including secondary mutations (e.g., T790M and C797S), bypass pathway activation (e.g., MET amplification), and phenotypic transformations (e.g., epithelial–mesenchymal transition (EMT) or small cell lung cancer (SCLC) transformation), often limit the long-term efficacy of EGFR-TKIs [1,2,3,4]. Here, EGFR is linked to small cell lung carcinoma.