For instance, because knocking down CISD2 expression or targeting CISD2 with pioglitazone, as exemplified by Darash-Yahana and colleagues14, can lead to an imbalance in ROS homeostasis and an increase in oxidative stress, methods for inhibiting the action of CISD2 may be developed to assist in the eradication of lung cancer cells, or to function as sensitizers to enhance chemotherapy or radiotherapy, in a similar way to that proposed for the NRF2–KEAP1 scenario in lung cancer treatment41,42. The gene discussed is KEAP1; the disease is lung carcinoma.