Taken together, these findings–that, in our cohort, HBV RNA positive tumors were characterized by a near-complete absence of NFE2L2 mutations and an association between KEAP1 mutations and diminished survival in the limited subset of patients harboring these mutations–could suggest a functional distinction in the manner in which the oxidative stress response pathway is dysregulated in HBV-mediated tumorigenesis compared to non-HBV HCC. This evidence concerns the gene KEAP1 and hepatocellular carcinoma.