fig1

Figure 1. Conceptual roadmap linking liver injury, inflammation, and immune dysregulation to either cirrhosis or HCC: Chronic liver injury can diverge into two mechanistically distinct yet overlapping trajectories once acute inflammation becomes persistent. In the fibrogenic axis (blue, Pathway A), ongoing injury sustains exposure-associated chronic inflammation that matures into cirrhosis-associated immune dysfunction (CAIDS) and ultimately cirrhosis (timeline cues 1 → 2 → 3)^[55]. In parallel, the same chronic insult can trigger a mutation-driven, immunosuppressive axis (red, Pathway B): DNA damage and progressive immune exhaustion create a tumor-promoting micro-environment (TME), allowing hyperplasia, dysplasia, and progression to hepatocellular carcinoma (HCC) (cues 4 → 5). The “fork” after step 2 represents the point at which repair-dominant (fibrogenic) vs. mutation-dominant (oncogenic) programs dictate whether cirrhosis, HCC, or both emerge from the shared inflammatory milieu. CAIDS: Cirrhosis-associated immune-dysfunction syndrome; TME: tumor micro-environment. Created in BioRender. Alsudaney, M. (2026) https://BioRender.com/uvlt8j2.