In fact, data suggest that MYC promotes a variant subset of SCLC with lower expression of neuroendocrine markers and with more aggressive features, that could originate from ASCL1+ progenitor cells which, over time, transition to an ASCL1-low/NEUROD1-high state due to the indirect effect of MYC on NEUROD1 signaling (83). This evidence concerns the gene ASCL1 and small cell lung carcinoma.