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). The gene discussed is MYD88; the disease is bacterial infectious disease.