Exploring the relationship between NRF2 overactivation and drug resistance in cancer, Wang et al.33 previously demonstrated that the transient knockdown of NRF2, or its specific inhibition by KEAP1 overexpression, both strongly increased the susceptibility of lung cancer cells to different chemotherapics, including cisplatin, doxorubicin, and etoposide. The gene discussed is KEAP1; the disease is lung carcinoma.