Additionally, in a model of anti-glomerular basement membrane glomerulonephritis (anti-GBM GN), the Th17/IL-17 pathways were drivers of inflammation and autoantibody-induced renal injury; and the knockout or inhibition of IL-17 ameliorated these effects associated with decreased proinflammatory cytokines (145, 146). This evidence concerns the gene IL17A and ganglioneuroma.