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. This evidence concerns the gene MYD88 and ganglioneuroma.