When cells are stimulated by external stimuli, such as oxidative stress, infection, or physicochemical stimuli, they can activate the transcriptional activity of NF-κB and promote the acidification and degradation of IκB, thereby releasing NF-κB into the nucleus and binding to the κB site of the target gene, rapidly inducing target gene transcription and up-regulating the expression of various biomacromolecules, including inflammatory cytokines, chemokines, and apoptosis-related factors. Here, NFKB1 is linked to infection.