ACTA1 and Hepatic fibrosis: Progressive liver fibrosis represents one of the major consequences of chronic hepatic injury and is associated with the activation of hepatic stellate cells (HSCs) from a quiescent state into proliferative, α-smooth muscle actin (α-SMA)-positive myofibroblasts that produce a variety of extracellular matrix (ECM) proteins.1 Identification of mechanisms central to the development of liver fibrosis offers the potential to target these molecules in the development of antifibrotic therapies.