Recent studies by Banas et al. reported that cultured podocytes constitutively expressed TLR4 and produced chemokines in response to stimulation with LPS, and that TLR4 expression by podocytes may be critical in triggering glomerular inflammation in a model of membranoproliferative glomerulonephritis [22]. This evidence concerns the gene TLR4 and membranoproliferative glomerulonephritis.