FADD and RIPK1 can interact with MAVS (Figure 7),128 and FADD- and RIPK1-deficient cells are hypersensitive to viral infection owing to an inability to induce the transcription of key antiviral genes.35 Tschopp and co-workers elucidated the mechanistic basis of these findings and found that the antiviral RIG-1 signalling pathway bears a striking resemblance to the TNFR1 pathway.64, 129 They propose that following viral infection, a complex termed the ‘TRADDosome' (composed of TRADD, RIPK1 and FADD) forms on the mitochondrial membrane via MAVS. The gene discussed is TNFRSF1A; the disease is viral infectious disease.