A) Immunoblot analysis of EGF-induced Erk and Akt pathway activation in NB7 cells lacking caspase-8 re-constituted with empty vector (E.V.), the DEDs alone (DEDs) or the “caspase domain” of caspase-8 (Casp. Dom.) (lanes 1–3, respectively). B) Immunoblot analysis of EGF-induced Erk and Akt pathway activation in NB7 cells lacking caspase-8 re-constituted with empty vector (E.V.), the catalytically inactive point mutant (C360A) or the C360A/Y380F dual mutant of caspase-8 (C360A/Y380F) (lanes 1–3, respectively). C) Immunoblot analysis of EGF-induced Erk pathway activation in NB7 cells lacking caspase-8 re-constituted with empty vector, the catalytically inactive point mutant (C360A) or the C360A/Y380F dual mutant of caspase-8 (as in Fig 5B) with or without sodium orthovanadate (200 µM) as described (lanes 1–4, respectively). D) Simplified schematic depiction of the proposed model of the critical role for caspase-8 in EGF induction of Erk pathway signaling events.