In the presence of the aforementioned NF-κB signaling, MSU crystals promote cytokine production via antigen-presenting cells (APC), specifically dendritic cells (DC), driving polarization of IL-17A-producing CD4-positive T helper cells (TH17), which in turn are essential for crescentic glomerulonephritis because they drive neutrophil-mediated inflammation [22,23,24,25]. This evidence concerns the gene NFKB1 and crescentic glomerulonephritis.