These are all regulated by NF-κB transcription factors and their expression might have been expected to be enhanced given the suppressive effect of the N1L protein on this pathway.37 Based on their well-characterized functions, enhanced production of KC (mainly from infected tumor cells) and GCSF was most likely to be responsible for the enhanced infiltration of i.t. neutrophils seen in vivo following VVΔTK∆N1L infection. The gene discussed is CSF3; the disease is neoplasm.