In their genetically engineered ERPMT mouse model of SCLC transformation, Gardner et al. elegantly demonstrated that Myc over-expression cooperates with Rb1 and p53 loss to drive reprogramming of EGFR-mutant LUAD into a highly undifferentiated, stem/progenitor-like state following blockade of EGFR activity [53]. Here, MYC is linked to small cell lung carcinoma.