This hypothesis is consistent with the model that inflammatory killing of tumor cells through viral oncolysis will recruit antigen presenting cells (APC) to the tumor site, release high loads of tumor associated antigens (TAA), and facilitate presentation of these TAA to CD8 and CD4 T cells in the draining lymph nodes, thereby generating systemically active anti-tumor T cell immunity26, 27, 28, 29, 30, 31, 32. The gene discussed is CD4; the disease is neoplasm.