Although some prior studies have suggested that inactivation of the tumor protein p53 (TP53) and retinoblastoma 1 (RB1) genes might be associated with the transformation of EGFR-mutated non-small cell lung cancer (NSCLC) to SCLC following TKI therapy (13, 14), the full clinicopathological characteristics and underlying molecular mechanisms of this transformation remain largely unexplored. This evidence concerns the gene EGFR and non-small cell lung carcinoma.