Corroborating evidence includes (i) frequent relapses due to viral or bacterial infection, (ii) LPS-induced proteinuria and podocyte foot process effacement in mice lacking T and B cells, (iii) expression of TLRs and the TLR4/MyD88/NF-κB signaling pathway in human podocytes, and (iv) absence of inflammatory cells, complement proteins, or immune deposits (except occasional IgM) in MCD and FSGS (13–15, 33–36). This evidence concerns the gene TLR4 and focal segmental glomerulosclerosis.