Several studies in mouse models of neurodegenerative diseases have reported downregulation of the NF-kB pathway in response to long-term treatment with UA, with decreased levels of IL-1β, IL-6, IL-12, and IFN-γ resulting [3], as well as activation of the nuclear factor-erythroid 2-related factor 2 (Nrf2) pathway by UA, which can protect cells from oxidative stress during cerebral ischemia [27,28]. This evidence concerns the gene NFKB1 and neurodegenerative disease.