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. The gene discussed is TP53; the disease is non-small cell lung carcinoma.