TLRs can be stimulated by multiple invading exogenous pathogens through PAMPs and recognized endogenous ligands released by necrotic cells through damage-associated molecular patterns (DAMPs), containing high-motility group box-1, heat shock protein, fibrinogen, heparin sulfate, fibronectin, hyaluronic acid, and double- and single-strand RNA, that have been demonstrated to promote tumor cell survival and proliferation by targeting various TLRs expressed on tumor cells and subsequently activate the key downstreams signaling pathways of TLRs to affect the development of HCC [26]. Here, FN1 is linked to neoplasm.