In EGFR‐mutant lung adenocarcinoma (LUAD), the combined inactivation of TP53 and RB1 significantly elevates the risk of small‐cell transformation following the development of resistance to EGFR tyrosine kinase inhibitors [3], while loss of RB1 alone is insufficient to induce neuroendocrine differentiation [11]. The gene discussed is EGFR; the disease is lung adenocarcinoma.