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 The gene discussed is TGFB1; the disease is Hepatic fibrosis.