In fact, serum and liver MCP-1 levels are increased in NASH patients [58], whereas in animal NASH models, the genetic deletion of MCP-1 and CCR2 or the inactivation of CCR2 reduces macrophage infiltration, attenuates obesity, and improves both insulin resistance and hepatic steatosis [51,52,59]. Here, CCR2 is linked to metabolic dysfunction-associated steatohepatitis.