Disturbed antioxidant efficiency as a result of infection promotes increased generation of ROS, which may regulate the degradation of IκBα, which plays an important role in the activation of NFκB signaling pathways, causing the release of p50 and p65 dimers and their translocation to the nucleus for the transcription of inflammatory genes, including TNFα [39,40]. Here, NFKB1 is linked to infection.