Indeed, our findings support this hypothesis: infection of tumor cells, both in vitro and in vivo, with a VACV containing deletions in the thymidine kinase (TK, J2R) and cGAMP nuclease (poxin, B2R) genes resulted in activation of the IRF3 pathway, triggering transcription of genes encoding inflammatory proteins, particularly type I interferons. The gene discussed is BDKRB2; the disease is infection.