In response to liver injury, quiescent HSCs trans-differentiate into myofibroblast-like cells (activated HSCs) which express alpha-smooth muscle actin (α-SMA) and a variety of pro-fibrogenic cytokines and proteins, including TGFβ1/2, cellular communication network 2 (CCN2), platelet derived growth factor, fibroblast growth factor, and tissue inhibitors of metalloproteinases that promote remodelling of extracellular matrix and contribute to liver fibrosis and cirrhosis.2 This evidence concerns the gene ACTA1 and Hepatic fibrosis.