The thymidine kinase (TK) gene deletion imparts tumor selectivity as cellular TK expression in cancer cells is constitutively higher than normal cycling cells.18 In many platforms, specificity may be supported by viral growth factor (VGF), ribonuclease reductase (RR; F14L), N1L or other gene deletions.19 20 Additionally since non-cancer cells use apoptosis as an antiviral defense mechanism, deletion of anti-apoptotic genes (SPI-1, SPI-2, F1L, and N1L) in VVs can increase selectivity towards tumor cells and enhance antitumor effects.21–23. The gene discussed is SPI1; the disease is neoplasm.