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Acute-on-chronic liver failure (ACLF) represents one of the most devastating syndromes in hepatology, characterised by acute decompensation of cirrhosis, multiorgan failure and high short-term mortality.1 Dysbalanced activation of innate and adaptive immune cells, along with inflammatory cytokines and immune paralysis with subsequent metabolic dysfunction, is a key factor determining the prognosis of liver and multiorgan failure in ACLF.2 However, most of these insights have been gained from large European and American consortia, in which alcohol or non-viral causes predominate the aetiology of the underlying liver disease and in which infections and alcohol-related hepatitis represent precipitating triggers.3 In Asia, chronic hepatitis B virus (HBV) infection is the leading aetiology of cirrhosis, and ACLF is often triggered by acute hepatitis flares due to HBV reactivation.4 In Gut, Liang et al provide important new insights on the dynamic immune alterations that drive disease progression by applying single-cell multimodal technologies to chart the immune landscape across HBV disease states.5 Their work offers a high-resolution view of cellular dysfunction during progression from chronic HBV to cirrhosis and finally ACLF, highlighting both pathogenic pathways and potential opportunities for novel biomarkers or interventions.