Chronic hepatitis B virus （HBV） infection is a major cause of hepatocellular carcinoma （HCC）， with a population-attributable fraction of 57.1% for HCC globally and 76.1% for HCC in China. Identifying the early molecular mechanisms of HBV-driven hepatocarcinogenesis can facilitate precise HCC prevention. Persistent HBV replication， HBV mutation， HBV integration， and the synergistic interplay among them are the main mechanisms of HBV-driven hepatocarcinogenesis. HBV replication activates and sustains a chronic hepatic inflammatory microenvironment， providing conditions for accumulation of viral mutations； under the conditions of chronic inflammation， inflammatory factors cause the imbalance between apolipoprotein B messenger RNA editing enzyme catalytic polypeptide-like 3B and uracil-DNA glycosylase， which promotes HBV mutations and human genomic mutations and enhances the carcinogenic effect of HBV mutations， and the inflammatory microenvironment can promote dedifferentiation of mutated cells and acquisition of stemness； HBV genome integration can cause “gate-keeper” mutations including telomerase reverse transcriptase （TERT） promoter mutation， thereby triggering chromosomal instability and epigenetic reprogramming. The three events of HBV replication， mutation， and integration work synergistically under the evolutionary principle of “variation-selection-adaptation” and jointly drive the development and progression of HCC. The high-risk HBV mutation profile， circulating HBV integration fragments， and the TERT promoter mutations can be used to guide precision HCC prevention via antiviral prophylaxis and assist in early screening and monitoring of postoperative recurrence， which provides a scientific basis for refining stratified prevention and control strategies against HCC.