The swift engulfment of apoptotic bodies by phagocytic cells is essential in orchestrating normal tissue homeostasis and in protecting tissues from inflammatory injury due to noxious release from dyng cells [l]. This is in contrast with the inflammatory response that results from exposure to necrotic corpses, whose clearance is also a task of professional phagocytes. It is not known, however, whether this dualism derives from the engagement of different mechanisms of recognition by a phagocyte challenged with a necrotic or apoptotic particle. More generally, in fact, little is known about the regulation of necrotic, as opposed to apoptotic, engulfment. In Caenorhabditis elegans, several genes working on two parallel pathways have been implicated in the process of engulfment of cells dying by apoptosis on the basis that their mutations lead to abnormal persistence of corpses [2, 3]. Among them, ced-5, assigned to a unique pathway with ced-2 and ced-10, has been identified as the nematode homologue of the cytoskeletal organizer DOCK180 [4]. Ced-6 works as a putative adaptor along a second pathway together with ced-1 and ced-7; the latter has been identified recently as an ATP Binding Cassette (ABC) transporter whose function has not yet been elucidated [561.