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Apoptosis is a highly conserved program of cell death in multicellular organisms that is central to their homeostasis. Defects in apoptosis are associated with cancer as well as neurodegenerative and autoimmune diseases.1 There are two ways apoptosis can be induced: intrinsic and extrinsic. The intrinsic pathway is triggered via changes in the mitochondria, the extrinsic pathway via stimulation of the so-called death receptors (DRs). All members of the DR family are expressed on the cell membrane and characterized by the presence of a death domain (DD) playing a central role in the transduction of the apoptotic signal. So far the DR family comprises TNF-R1, CD95/Fas/APO-1, DR3, TNF-related apoptosis-inducing ligand-receptor (TRAIL-R1), TRAIL-R2 and DR6.1 The central event in DR signaling is the formation of the death-inducing signaling complex (DISC). The DISC comprises oligomerized, probably trimerized receptors, the adaptor protein FADD, procaspase-8, procaspase-10 and c-FLIP.1