Previous studies have shown that patients with gout have increased levels of circulating Th17 cells,48 and that urate crystals in combination with an NF-κB priming signal induce Th17 polarization in vitro.49 Moreover, in MSU-induced joint inflammation in mice, blocking IL-17 attenuated the recruitment and activation of immune cells, as well as joint inflammation.50 Here, NFKB1 is linked to gout.