Combined with the data on the role of JAM-A in reovirus-mediated CAF killing, this points to a potential bimodal mechanism of action of targeting JAM-A expressing fibroblasts with reovirus that would enable (1) lysis of JAM-A expressing desmoplastic stromal cells and (2) serve as a conduit for OV replication and subsequent infection of desmoplastic-adjacent tumor cells. This evidence concerns the gene F11R and neoplasm.