Seeing that some HERVs could be transcriptionally activated by HDACi treatment, we asked the question whether this effect might be exploited in analogy to SaK to induce selective cancer cell death in two ways: by forcing the expression of HERV envelope proteins in the cell membrane and targeting them with specific antibodies or CART systems, and second, by recruiting the cell’s own innate immune response via agonization of TLR7/8 receptors, which recognise viral signatures. The gene discussed is ERVW-1; the disease is cancer.