Recently, a murine model of SCLC combining Trp53 and Rb1 knockout with Myc overexpression revealed that SCLC-N tumors could arise from SCLC-A precursor lesions14, suggesting lineage plasticity fueled by Myc. Consistent with this idea, PSCCE-N tumors were also associated with MYC amplification. This evidence concerns the gene RB1 and small cell lung carcinoma.