In response to liver damage signals, KCs are activated by LPS, fatty acids, and oxidative stress and interact with the classical TLR4/MyD88/NF-κB signaling pathway to differentiate toward the M1 phenotype, resulting in increased secretion of TNF-α, IL-6, IL-8, and iNOS, which promote inflammation and NAFLD progression. Here, TBCE is linked to metabolic dysfunction-associated steatotic liver disease.