Consequently, this should lead to: (1) higher virus load in the tumor, (2) more virus-mediated lysis of cancer cells, which produce TIL enhancing cytokines, and, eventually, (3) better therapy results with more activated and mature TILs fighting the tumor, and (4) TNFa and IL-2 would also recruit further virus-loaded TILs in a self-amplifying loop. The gene discussed is IL2; the disease is neoplasm.