Our identification of a novel panel of miRNAs in HCCs linked to chronic alcohol exposure, coupled with our analyses correlating miR-944 with mutations in Wnt-activator CTNNB1 [22] and miR-223 with patient survival and presence of residual tumor (Fig 1C–1E), suggests that alcohol-mediated dysregulation of miRNAs in HBV+ HCC modulates central pathways and contributes to clinically relevant phenotypes in HCC patients. This evidence concerns the gene CTNNB1 and neoplasm.