Liver failure is the major cause of death in alcoholic steatohepatitis (ASH). In experimental hepatitis, granulocyte‐colony stimulating factor (G‐CSF) mobilizes hematopoietic stem cells, induces liver regeneration, and improves survival. We studied the short‐term effects of G‐CSF on CD34+ stem cell mobilization, liver cell proliferation, and liver function in patients with ASH. Twenty‐four patients (mean age 54 years) with alcoholic cirrhosis [Child‐Turcotte‐Pugh score 10 (7–12)] and concomitant biopsy‐proven ASH [Maddrey score 36 (21‐60)] were randomized to standard care associated with 5 days of G‐CSF (10 μg/kg/day, group A, n = 13) or standard care alone (group B, n = 11). Serial measurement of CD34+ cells, liver tests, cytokines [hepatocyte growth factor (HGF); tumor necrosis factor α; tumor necrosis factor‐R1; interleukin‐6; alfa‐fetoprotein], and ¹³C‐aminopyrine breath tests were performed. Proliferating hepatic progenitor cells [HPC; double immunostaining (Ki67/cytokeratin 7)], histology, and neutrophils were assessed on baseline and day 7 biopsies. Abstinent alcoholic patients with cirrhosis served as controls for immunohistochemistry. G‐CSF was well tolerated. At day 7, both CD34+ cells (+747% versus −6%, P < 0.003), and HGF (+212% versus −7%, P < 0.03) increased in group A but not in group B. Cytokines and aminopyrine breath test changes were similar between groups. On repeat biopsy, a >50% increase in proliferating HPC was more frequent in group A than in group B (11 versus 2, P < 0.003). Changes in Ki67+/cytokeratin 7+ cells correlated with changes in CD34+ cells (r = 0.65, P < 0.03). Neutrophils and histological changes were similar in both groups. Conclusion: G‐CSF mobilizes CD34+ cells, increases HGF, and induces HPC to proliferate within 7 days of administration. Larger trials would be required to determine whether these changes translate into improved liver function. (HEPATOLOGY 2008.)