Since emerging pieces of evidence indicate that the CCL2/CCR2 axis is involved in fibrotic diseases [39], and since we have previously demonstrated that GILZ deficiency is associated with elevated CCL2 expression and recruitment of CCL2-sensitive immune cells in the liver of GILZ KO mice compared to controls, in a murine model of liver fibrosis [40], we checked the mRNA expression levels of CCL2 chemokine and its receptor, involved in fibrotic progression. The gene discussed is CCL2; the disease is Hepatic fibrosis.