NFKB1 and gout: This combination of reduced renal excretion and increased UA production leads to a state of hyperuricemia, setting the stage for the crystallization of monosodium urate in joints, a hallmark of gout.[37] Another crucial pathway linking hypertension to gout involves oxidative stress and inflammation.[38] Hypertension contributes to the activation of various inflammatory signaling pathways, including the NF-κB and IL-6 pathways, which increase the production of pro-inflammatory cytokines.