As TLRs are among the most important sensors of an inflammatory environment, it was unexpected that a knockout of the central adaptor protein MYD88 in podocytes did not result in a significant alteration of experimental GN, especially as a podocyte-specific knockout of the NF-κB adaptor NEMO resulted in a significant attenuation of GN5. The gene discussed is IKBKG; the disease is ganglioneuroma.