However, hyperactivation of NF-κB signaling may lead to immunopathology and diseases, as observed in LPS-mediated TLR4 activation during Gram-negative sepsis.73 The results presented in the present study provide evidence that the DUB OTUB1 critically supports canonical NF-κB activation in DCs and mediates DC-dependent protection in infectious disease, but augments immunopathology upon LPS challenge. This evidence concerns the gene NFKB1 and infectious disease.