Excessive alcohol intake induces liver inflammation and cell death. We work on the pathomechanism by which stellate cells (HSCs) and hepatocytes communicate injury signals triggering local immune responses. We employ bench-to-bedside and bedside-to-bench approaches and found that the non-phagocytic NOX4 was induced in early alcoholic liver injury in patients. Using in vivo and in vitro approaches we showed that NOX4 promoted recruitment of inflammatory cells and production of proinflammatory cytokines by affecting CCR2/CCL2 mRNA stability. We are now developing novel assays to address disease heterogeneity, and patient outcomes.