Moreover, Sparstolonin B obviously inhibited Kupffer cell activities as evidenced by the decrease in MCP-1 and CD68 levels with concomitant suppression of macrophage infiltration via blocking NADPH oxidase-driven TLR4 trafficking to the lipid rafts in NASH (Dattaroy et al., 2016). Here, CCL2 is linked to metabolic dysfunction-associated steatohepatitis.