Concerning liver cancer, ROS generated by hypoxia along the edge of tumor growth presents a dual role: (i) it promotes carcinogenesis by activating NF-κB and HIF1α, which favor cancer cell survival, angiogenesis, and tumor expansion; (ii) on the other hand, after mitochondrial GSH depletion, it shifts hypoxia from a cancer-promoting to a cancer-killing environment [27–29]. Here, HIF1A is linked to neoplasm.