This UL76-mediated increase in IL-8 production was shown to be dependent on the cellular kinases Ataxia-telangiectasia mutated (ATM) and IKKβ; however, ablation of ATM expression in cells or of the key endonuclease motif amino acids present in UL76 failed to completely restore IL-8 production back to wild-type levels during infection [103], implying that additional aspects of NFκB signaling might be contributing to this phenotype. Here, CXCL8 is linked to infection.