In this study, the prophylactic treatment with β-Lap mitigates the excessive release of TNF-α, IL-1β in serum, and peritoneal cavity of animals 24 hours after CLP, suggesting a polarization to M2 phenotype, which is associated with the downregulation of nuclear factor kappa B (NF-κB) pathway that in sepsis promotes excessive release of IL-1β and TNFα, inflammatory cytokines central to the pathophysiology and partly involved in the pathogenesis of multiple organ failure [45]. The gene discussed is IL1B; the disease is Sepsis.