However, TLR4-specific antagonist TAK-242 significantly reverted MFG-E8 knockout-aggravated NASH phenotype, as indicated by decreased lipid droplet formation and TG synthesis, and weakened inflammatory cytokine production (Figure 8), suggesting that TLR4 might participate in the function of MFG-E8 on modulating NASH progression. Here, TLR4 is linked to metabolic dysfunction-associated steatohepatitis.