Using L. monocytogenes as a bacterial model pathogen, which induces a type I IFN response that completely depends on TBK1 and IKKε in THP1 monocytes, we could show that IKKε regulation by TBK1 is essential for host responses to bacterial infection: Cells that lack active TBK1 but fail to upregulate IKKε showed a strongly diminished type I IFN and IFN-stimulated gene expression in response to bacterial infection compared to TBK1-deficient cells that are able to induce IKKε expression. The gene discussed is TBK1; the disease is bacterial infectious disease.