Hepatic fibrosis is the final common pathway for a multitude of liver injuries. Viral-, immune-, or toxin-mediated liver injuries all result in expansion of the extracellular matrix with distortion of hepatic architecture and development of cirrhosis. Originally thought of as a one-way street, hepatic fibrosis now is recognized as a dynamic process with the potential for significant resolution. Authors in this issue address the genetic determinants of fibrosis, oxidant stress, cellular contractility and vasoregulation, as well as relationships between stellate cell activation, progenitor cells and hepatic regeneration. Current and future antifibrotic therapies are also discussed.