In addition, the exon 2 in the Nrf2 locus is recurrently lost via alternative splicing and this contributes to the production of NRF2 isoform lacking the Neh2 domain, suggesting an alternative mechanism how NRF2 is activated in lung cancer cells that do not bear mutations in the KEAP1/NRF2 pathway (Goldstein et al., 2016). This evidence concerns the gene KEAP1 and lung carcinoma.