Immunofluorescence assays of resected tumor tissue identified SipL as a hepatic factor supporting HCV infection and replication, in combination with CD81 and other cofactors in an otherwise non-permissive cell line.[19] Further studies on mouse hepatomas verified that co-expressed human CD81 and SipL in Hepa1-6cells are permissive for HCV infection and replication. Here, ADI1 is linked to neoplasm.