In lung cancer, the co-occurring mutations in KEAP1, NFE2L2, or cullin 3 (CUL3) observed in 7% of non-small cell lung cancer (NSCLC) patients with EGFR (Epidermal Growth Factor Receptor) mutations indicate the activation of the NRF2 pathway as an acquired mechanism, leading to the resistance to usually beneficial EGFR-tyrosine kinase inhibitor therapy [55]. The gene discussed is EGFR; the disease is lung carcinoma.