Especially, H-HBV-SITE-1 could not activate 113 genes, including KRAS, ATF2, ITGA2, EGFR, BUB1B, and CDC7, which were enriched in terms of tumorigenesis by B-HBV-SITE-1 (Fig. 3D and Fig. S3), and most of them accounted for poorer survival for HCC patients [62]. Here, KRAS is linked to hepatocellular carcinoma.