Sepsis induction reduced NF-κB and SOD2 protein expression but increased their acetylation (Figures 4A–E), and this was accompanied by an increase in proinflammatory cytokines (TNF-α/IL-6/IL-10; Figures 4F–H) and oxidative stress (indicated by reduced SOD2 activity, GSH content, GSH/GSSG ratio, and CAT activity; Figures 4I–L). The gene discussed is NFKB1; the disease is Sepsis.