ACTA1 and Hepatic fibrosis: Although liver fibrosis is caused by a variety of etiologic agents, including chronic viral hepatitis, alcohol toxicity, autoimmune disease, and hereditary metabolic disorders, it is now generally accepted that a central pathologic mechanism underlying liver fibrosis is the generation and proliferation of smooth muscle α-actin (α-SMA)-positive myofibroblasts of periportal and perisinusoidal origin that arise as a consequence of the activation of hepatic stellate cells (HSCs) [1–3,4].