Thus, although we could not exclude the potential role of neutrophils-derived tlr4 in the induction phage of anti-GBM GN because lysM promoter-driven Cre recombinase also results in functional deficiency of tlr4 in neutrophils, the massive macrophage infiltration and the majority of macrophage TLR4 deletion (85%) during progressive crescentic GN may reveal a critical role for macrophage-dependent TLR4, rather than neutrophil-derived TLR4, in anti-GBM GN. The gene discussed is TLR4; the disease is glioblastoma.