Jiang et al. [30] confirmed that when ASCL1 was successfully overexpressed with SV40 large T-antigen, it could synergistically inhibit retinoblastoma protein and p53 to promote the development of aggressive adenocarcinoma with NE characteristics; however, in the developing mouse lung, knockout of ASCL1 resulted in specific ablation of lung NE cells. This evidence concerns the gene ASCL1 and adenocarcinoma.