These observations led to the speculative notion that the impairment of aberrant molecular KEAP1/NRF2 and NOTCH crosstalk by genetic and epigenetic factors in these genes might impact the complex landscape of SCLC and exert a critical role in oxidative stress, metabolism, and cell fate determination of neuroendocrine lung tumors and SCLC. This evidence concerns the gene KEAP1 and small cell lung carcinoma.