The elevation of pro-inflammatory cytokines can, in turn, upregulate inducible nitric oxide synthase(iNOS) by activating NF-κB, leading to an increase in nitric oxide (NO), which can pose a threat to neurons, thereby exacerbating AD neuropathologically primarily through two mechanisms: (1) NO can promote the activation of NF-κB pathway by regulating neuronal migration during development, thus aggravating CNS damage and exacerbating AD disease progression [65]. Here, NFKB1 is linked to Alzheimer disease.