It therefore seems possible that stimulation of the RLR pathway after bacterial infection promotes TBK1 activation by OPTN at the Golgi apparatus and that, on the one hand, p-TBK1S172 triggers the production of type I IFNs and, on the other, the active kinase phosphorylates OPTN to induce the xenophagy of the invading bacteria. This evidence concerns the gene DHX58 and bacterial infectious disease.