Importantly, genetic or pharmacologic inhibition of MCP-1 or CCR2 improved NASH and IR in different mouse models of NAFLD [HFD, carbon tetrachloride (CCl4), MCD-diet, high-fat, high-sucrose diet] [138–140], with more prominent improvement shown in CCR2 versus MCP-1 blockade, probably because CCR2 is also a receptor for other chemokines, i.e., CCL7, CCL8, and CCL13 [129]. The gene discussed is CCL2; the disease is metabolic dysfunction-associated steatotic liver disease.