Ectopic overexpression of N1ICD in the mouse lung alveolar epithelium leads to the formation of adenomas with an increased Myc level and, after a long latency period, adenocarcinomas.24 The tumorigenicity of N1ICD can be augmented by the co-overexpression of MYC. 24 We used this mouse model to investigate the relationship between NOTCH activation and metabolic reprogramming in NSCLC. This evidence concerns the gene MYC and non-small cell lung carcinoma.