(1) Upon liver damage, hepatic stellate cells undergo a process defined as activation (Fig. 1), that enables them to acquire a myofibroblastic phenotype. The biological actions of myofibroblasts are pivotal for liver tissue repair and fibrogenesis [1].(2) Activation of TGFb-dependent fibrogenic signalling in hepatic stellate cells. The source of TGFb is initially paracrine including hepatocytes, Kupffer cells, and platelets activated in response to hepatic injury [2].(3) At the same time TLR4 signalling in hepatic stellate cells is required for down-regulation of TGFb pseudoreceptor (and inhibitor) BAMBI in order to render hepatic stellate cells sensitive to TGFb signalling. Bacterial-derived LPS is currently considered to be the key fibrogenic TLR4 ligand; however, additional endogenous ligands from damaged and dying hepatocytes cannot yet be ruled out as playing a role [3].(4) TGFb signals generate transcriptional active pro-fibrogenic Smad2 and Smad3 complexes [2], but also stimulates collagen transcription in hepatic stellate cells via hydrogen peroxide and C/EBPb.