For example, HCV’s interference with BRG1 and BRM components shifts gene expression toward pro-inflammatory and oncogenic states, amplifying NF-κB and STAT3 signalling, which promotes fibrosis, inflammation, and genomic instability, accelerating HCC progression (Tonon, 2016; Pfefferlé and Vallelian, 2024). The gene discussed is NFKB1; the disease is hepatocellular carcinoma.