The result is an epigenetically-regulated transcriptional program involving secretion of TGF-β1, CTGF, p16, CCL2 and SA-β-gal, ultimately leading to a profibrogenic micro-environment, HSC activation, and enhanced liver fibrosis (Zhou et al., 2018; Elssner et al., 2019; Jalan-Sakrikar et al., 2019). This evidence concerns the gene TGFB1 and Hepatic fibrosis.