NFKB1 and hepatocellular carcinoma: This work (i) identifies a novel mechanism by which HBV-host interactions regulate lncRNAs involved in HCC progression; (ii) demonstrates that HBsAg drives hepatocarcinogenesis through the NF-κB/LINC00665 axis, thereby providing new mechanistic insights into the role of HBsAg in HCC (Fig. 7); (iii) explains, in part, clinical and in vivo observations supporting the role of HBsAg in HCC development, specifically in HBV inactivity; and (iv) supports previous studies advocating the use of LINC00665 as a therapeutic and prognostic marker in HCC (31, 44, 45).