When TNFR1 is mutated together with the mammalian NF-κB gene RelA, TNFR1/RelA-deficient mutant mice exhibit severe susceptibility to bacterial infection, hematopoietic defects and significant reductions in neutrophil recruitment to sites of injury and injected bacteria (Alcamo et al., 2001). This evidence concerns the gene TNFRSF1A and bacterial infectious disease.