However, unlike treatment with LPS/5z7 or high MOI Yersinia infection, which likely provide complete inhibition of TAK1 signaling, infection of macrophages at low MOI induced cell death that was additionally dependent on TNFR1, suggesting that in the absence of complete inhibition of pro-inflammatory signaling, TNF signaling amplifies cell death in response to Yersinia infection (Fig. 6c). This evidence concerns the gene TNFRSF1A and Yersinia infectious disease.