It is widely reported that TLR4 and its downstream signaling play a critical role in the pathogenesis of autoimmune glomerulonephritis.[1, 2, 3] Conventional TLR4 deletion has been reported to notably protect against renal dysfunction in experimental anti‐glomerular basement membrane (anti‐GBM) crescentic glomerulonephritis (cGN).[3] Indeed, TLR4 contributes to the early and transient glomerular neutrophil influx in the first 24 h in nephrotoxic antibody‐induced anti‐GBM GN.[1] However, the relative role of cell‐type specific TLR4, especially macrophage‐specific TLR4, remains largely unknown. The gene discussed is TLR4; the disease is glioblastoma.