Cancer cells adapt to the increased ROS during redox adaptation by upregulating the redox-sensitive transcription factors such as Nrf2, NF-κB, and HIF-1α.17 This offers undeniable advantages to cancer cells, including survival under stressful conditions, metastasis, and chemoresistance.3–5 Therefore, disruption of the redox adaptation therapeutically targets the cancer cells via pro-oxidant therapy.18 This evidence concerns the gene HIF1A and cancer.