TLR4 and Sepsis: Endotoxin initiates sepsis-related inflammation via the TLR4 which requires lipopolysaccharide binding protein (LBP) for activation.[7] TLR4- myeloid differentiation primary response protein 88 (MyD88) and TLR4-Toll/IL-1 receptor domain-containing adaptor-inducing interferon-β (TRIF) pathways are involved in these mechanisms, highlighting the complexity of the role of endotoxin in sepsis pathogenesis and the challenges in recognizing it for precise therapeutic interventions.