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Hepatocellular carcinoma (HCC) is a leading cause of cancer mortality worldwide, with chronic hepatitis B virus (HBV) infection a major etiological factor. While microRNAs have been extensively studied in HCC, the role of PIWI-interacting RNAs (piRNAs) is at the beginning. Here, a comprehensive analysis was applied on small RNA sequencing data to compare piRNA expression in HBV-related HCC tumors, HBV-infected non-tumor liver, and normal liver tissue. RNA reads were aligned with Rsubread and quantified piRNAs using featureCounts, identifying differentially expressed piRNAs with DESeq2. In HBV-HCC versus normal liver 11 piRNAs found to be significantly dysregulated (5 up, 6 down), including a 9.9-fold upregulation of hsa-piR-32885 and 5.3-fold downregulation of hsa-piR-28734. Comparing HBV-HCC to HBV-infected liver revealed 17 differentially expressed piRNAs, with hsa-piR-432 most strongly upregulated. HBV-infected versus normal tissue showed 22 dysregulated piRNAs (21 down, 1 up), especially hsa-piR-432 was 21-fold down. These stage-specific changes suggest dynamic piRNA regulation during HBV-driven hepatocarcinogenesis. Many of the identified piRNAs are novel in the HCC context. Accordingly, hsa-piR-32885 has not been previously linked to liver cancer, though piR-Hep1 was found upregulated in ~47% of HCCs. The switch in hsa-piR-432 (down in HBV infection, up in HCC) highlights candidates for biomarkers or functional regulators. This study concludes that piRNA profiling in HBV-HCC uncovers novel markers and pathways. Future work will validate these piRNAs in larger cohorts and explore their regulatory targets. These findings support piRNAs as emerging players and biomarkers in HBV-associated HCC.