['Hepatic stellate cells (HSCs) are the principal cells responsible for the development of hepatic fibrosis and cirrhosis. During the fibrotic process, HSCs undergo proliferation and transdifferentiation from a quiescent to myofibroblast-like phenotype. The fate of myofibroblast like HSCs includes apoptosis or reversion back to a quiescent phenotype. The mechanisms involved in the apoptotic process of HSCs have yet to be determined. The purpose of the present study is to determine the effects of extracellular signal-regulated kinases (ERKs) phosphorylation on the apoptosis of HSCs induced by staurosporine.', 'We used Western blot and flow cytometry to detect the expression level of ERK and cell apoptosis status in four rat hepatic stellate cell lines (CFSC-8B, -2G, -3H and-5H).', 'Each hepatic stellate cell line had a distinct morphology consistent with their expression level of α-SMA and that CFSC-8B cells had the highest α-SMA expression. Although all four cell types expressed similar levels of ERK1/2, phosphorylation levels were significantly higher in CFSC- 8B and CFSC-2G than in CFSC-3H and CFSC-5H cells. When CFSC-8B cells (high ERK1/2 phosphorylation) and CFSC-5H cells (low ERK1/2 phosphorylation) were employed to examine staurosporine-induced apoptosis, CFSC-8B cells were significantly more sensitive. Staurosporine further increased ERK1/2 phosphorylation in both cell lines.'] Does extent of extracellular signal-regulated kinases phosphorylation determine the sensitivity of hepatic stellate cells to staurosporine-induced apoptosis?