The liver possesses an extraordinary regenerative capacity that is triggered upon death of parenchymal cells or after partial liver resection. This fundamental response likely evolved to protect the organ and the organism from endogenous and exogenous toxins and thus preserve systemic metabolic homeostasis.1 A number of mediators involved in the onset and termination of liver regeneration have been identified over the years, and these where categorized by the late Nelson Fausto into 3 types of interconnected pathways known as the cytokine, growth factor, and metabolic networks.