ACTA1 and Hepatic fibrosis: Once activated, HSCs transform into myofibroblasts, exhibiting increased proliferation, inflammation, and expression of profibrogenic genes such as alpha-smooth muscle actin (a-SMA), platelet-derived growth factor receptor beta (PDGFRβ), collagen type I alpha 1 chain (COl1A1), and tissue inhibitor of metalloproteinase 1 (TIMP1), thereby exacerbating liver fibrosis (14–17).