Similarly, IL-1 receptor antagonists were found to protect rats against the development of dimethylnitrosamine-induced liver fibrosis [46], and blocking IL-1 signaling was able to markedly attenuate alcohol-induced liver inflammation and pro-steatotic MCP-1/CCL2 levels in hepatocytes, and increases Toll-like-receptor-4-dependent upregulation of inflammatory signaling in macrophages [45]. This evidence concerns the gene CCL2 and Hepatitis.