In the context of sepsis, a significant elevation in oxidative stress arises primarily from the excessive generation of reactive oxygen species (ROS), a process largely mediated by proinflammatory cytokines such as interleukin-6 (IL-6), interleukin-1 (IL-1), and tumor necrosis factor-alpha (TNF-α) (55). The gene discussed is TNF; the disease is Sepsis.