In alcoholic liver disease, ethanol increasesgut permeability,leading to a scenario of endotoxemia driven by lipopolysaccharides(LPS) from commensal microbiota.24,25 LPS activatesKupffer Cells (KCs) through TLR426,27 and NF-κBexpression, resulting in the production of proinflammatory cytokines,including IL-1β and TNF-α.28 Our examination of cytokine levels in liver biopsies revealed thatthe alcoholic groups had significantly higher concentrations of TNF-αand IL-1β, coupled with a notable decrease in IL-10. The gene discussed is IL1B; the disease is serum lipopolysaccharide activity.