This is in contrast with lung cancer, where, in addition to the existence of well-characterised cell lines harbouring mutant hyperactive NRF2 (e.g., the lung cancer cell line A549), several models have been developed to study NRF2 hyperactivation, and a number of associated vulnerabilities have been identified by using KEAP1-deficient or loss-of-function mutant models [36,37,38,39]. This evidence concerns the gene KEAP1 and lung carcinoma.