In contrast, Ding et al. demonstrated that neuroendocrine differentiation induced by SMAD4 and/or RB1 inactivation in NSCLC models was not accompanied by increased expression of canonical SCLC therapeutic targets in cell line models, including BCL2 or DLL3, despite clear upregulation of neuroendocrine markers [43]. This evidence concerns the gene RB1 and non-small cell lung carcinoma.