Alcohol consumption impairs gut barrier functions, which consequently increases circulating endotoxemia and aggravates alcoholic steatohepatitis.[25] In the current work, the LJ or HKLJ treatments significantly reversed the negative effects of ethanol feeding, as indicated by a notable increase in the levels of lipopolysaccharide (LPS) and pro‐inflammatory cytokines (TNFα, IL‐6, and IL‐1β) in the circulation of mice (Figure 2A–D). The gene discussed is TNF; the disease is serum lipopolysaccharide activity.