During liver fibrosis regression, MFs convert into different cell fates, including inactivation, senescence and apoptosis 7-9, on the absence of pro-fibrotic factors, such as transforming growth factor-β (TGF-β), platelet-derived growth factor β (PDGF-β) and interleukin-17A (IL-17A), etc. 10-12. This evidence concerns the gene TGFB1 and Hepatic fibrosis.