These results demonstrate that HBXIP alone has little ability to modulate ROS, PPP flux, and ATP production unless Nrf2 is co-expressed, which is consistent with our previous study showing that HBXIP modulates ROS in breast cancer cells by competing with Nrf2 for binding with KEAP1 and promoting Nrf2 accumulation and activation9. The gene discussed is KEAP1; the disease is breast carcinoma.