Necrosis, a form of death characterized by rupture of the cell membrane, is 
closely interlinked with inflammation. Cellular components released during 
necrotic death can trigger inflammation. Conversely, inflammation often yields 
tissue damage and, as a consequence, cell death. Which occurs first--necrosis or 
inflammation--in specific in vivo situations is currently difficult to tell. A 
way out of this 'chicken-and-egg' conundrum may be found via the recent finding 
that both necrotic cell death and inflammation can be initiated by a distinct 
set of signaling proteins, the 'necrosome', that includes receptor-interacting 
protein (RIP)1, RIP3 and caspase-8. Further clarifying the function of these 
signaling proteins should make it possible to establish when they induce 
inflammation directly and when inflammation is caused by necrotic cell death.