While non-small cell lung cancers (NSCLC) harbor recurrent oncogenic mutations that can be targeted therapeutically (e.g. epidermal growth factor receptor (EGFR) or anaplastic lymphoma receptor tyrosine kinase (ALK)) [9], the most prevalent molecular alterations in SCLC are in TP53, RB1, and MYC, alterations without effective targeted therapies [10]. This evidence concerns the gene RB1 and non-small cell lung carcinoma.