These findings support a model in which, in the absence of TAK1 activity, TRIF-mediated activation downstream of TNF-R1 leads to the formation of a TRIF-dependent prodeath complex (prodeath TRIFosome) containing FADD, RIPK1, and caspase-8, which amplifies cell death via enhanced activation of GSDMD and executioner caspases (Fig. 1, G and H).