On the contrary, in the spontaneous recovery phase, we detected a downregulation of the elevated SDF-1α expression in the liver, accompanied by a progressive significant decrease in the expression of CXCR4 receptors in the liver and the percentage of the area of hepatic fibrosis, which may be due to the conversion and settling of CXCR4-positive cells as resident fibroblasts lose their phenotype over time [76]. Here, CXCL12 is linked to Hepatic fibrosis.