KRAS activity confers in NSCLC chemoresistance also by upregulating NRF2 through the link with TPA response element (TRE) located in exon 1 of the NFE2L2. In the same context of resistance to target therapy, it is possible that NFE2L2 mutations can contribute to survival under crizotinib treatment and can allow the cells to acquire additional resistance mutations over time. Here, NFE2L2 is linked to non-small cell lung carcinoma.