To assess the inflammatory response of both WT and nfκb1−/− mice we determined the levels of key pro-inflammatory proteins (TNF-α, IL-6, S100A8 and S100A9) which are known downstream targets for NF-κB as well as recognised contributors to GN disease progression.11, 12, 13 TNF-α, S100A8 and S100A9 gene expression in kidney was upregulated 2 h after NTS challenge in both WT and nfκb1−/− (Figures 3a) in comparison with WT saline injected animals. The gene discussed is NFKB1; the disease is ganglioneuroma.