NFKB1 and gout: AGA mainly triggers an inflammatory response due to urate deposition in local tissues, and current in vitro studies on gout are often explored on macrophages, neutrophils.[61] GA is known to activate the NF-κB and AP-1 signaling pathways, enhancing the secretion of pro-inflammatory cytokines such as IL-17, TNF-α, and IL-1β.[61,62] In the IL-17 signaling pathway, IL-17 binds to the receptor and activates downstream NF-κB and MAPK pathways, resulting in increased levels of TNF-α and IL-6.